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nflammator

LIST Osted in alphab

Abstra

P-1. Am

P-2. Lathrough

P-3. Thprotein

P-4. Hugastroin

P-5. Gapopto

P-6. A

P-7. Stdifferen

P-8. Imkinase-format

P-9. Thlimit in

P-10. Thyperte

P-11. Hcells

P-12. Acolorec

P-13. Gprolifer

P-14. Tdelamin


4

F ABSTRAbetical order

act Title:

melioration of

actobacillus reuteh orphan rece

he associationn kinase signal

uman intestinntestinal virus

fi1 functions aosis in colorect

novel mediato

ool microbiomntial arginine m

mpaired rotavi-inhibited cellstion

he microbiota nflammatory T

The role of theension

Human gut mi

Attenuation ofctal cancer by

Glucagon-like ration in intes

The cytoskeletnation in prein


Diseases in 2

ACTS r by author.)

f experimenta

teri DSM 1793eptor RORα/γ

n of Krüpple-liling in normal

nal enteroid cus infection

as a potential tal cancer cell

or of chronic

me compositiometabolism in

irus viroplasms provides new

a conditions CT cell response

e gut microbio

icrobiota alter

f colonic inflaprobiotic Lac

peptide-2 repstinal stem cell

tal regulator pnvasive pancr


al NEC by sur

8 suppresses Tγ

ike factor 5 anl intestinal pro

ultures: A new

tumor supprels

pancreatitis

on and predicn a multi-natio

m formation anw clues into ce

CX3CR1+ mones in the intes

ome in obstru

r intestinal mu

ammation and ctobacillus reuter

programs glucls

p120 catenin sureatic cancer

um:

rfactant protei

TH17 cell diffe

nd mitogen-acoliferation

w functional m

essor by induc

cted function ronal cohort of

nd maturationellular lipid dr

nonuclear phatine

uctive sleep ap

ucus in HT29-

inflammationri

ose metabolis

uppresses epit

in-A

ferentiation

ctivated

model of

cing

reflect f women

n in protein roplet

agocytes to

pnea induced

-MTX-E12

n-associated

sm for

thelial cell

Page:

21.

22.

23.

24. J

25.

26.

27.

28.

29.

30.

31.

32. J

33.

34.

35.

Tex 6th Fron

Name and InGirish S. HireClinical PostdTexas ChildreKendal HirscProfessor Baylor CollegDiane Leigh HPredoctoral FBaylor CollegJoseph MichaAssistant ProBaylor CollegFaith Dorsey Clinical PostdBaylor CollegLi Jiao, M.D.,Assistant ProBaylor CollegCoreen L JohPostdoctoral Baylor CollegSunkuk KwonAssistant ProUT Health SEric Lloyd, PInstructor Baylor CollegYuan-Hung LGraduate StuBaylor CollegPankajini MalGraduate StuUniversity of Janielle P MayPh.D. CandidBaylor CollegAdrienne McNPostdoctoral Baylor CollegChristina MorPh.D. CandidBaylor CollegDorottya NagPostdoctoral Baylor Colleg


nstitution: emath, M.D. Mdoctoral Fellowen's Hospital hi, Ph.D.

ge of MedicineHutchinson, B

Fellow ge of Medicineael Hyser, Ph.Dfessor

ge of MedicineIhekweazu, M

doctoral Fellowge of Medicine, M.S., Ph.D. fessor

ge of Medicinehnson, Ph.D. Associate

ge of Medicinen, Ph.D. fessor cience Centerh.D.

ge of MedicineLo, M.S. dent

ge of Medicinellick, B.S., M.Sdent Houston ynard

date ge of MedicineNees, Ph.D., BAssociate

ge of Medicinerra

date ge of Medicinegy-Szakal, M.DAssociate

ge of Medicine


nflammator

AbsM.P.H. w

P-1diff

e

P-1info

B.A.

e

P-1the

D.

e

P-1actirele

M.D. w e

P-1ped

e

P-2indi

e

P-2in vi

r

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P-2cate

S. P-2

e

P-2recu

B.A.

e

P-2aviu

e P-2

D.

e

P-2feca


5

stract Title:

5. Unbiased pferential expre

6. Gut dysfunormation betw

7. Norwalk vifecal microbi

8. Store-operaivated by rotavease of ER cal

9. Special condiatric recurren

20. Characterisividuals

21. Effects of Litro cell culture

22. Systemicallfate sodium-in

23. Cerebral smbiosis

24. SPDEF inhenin transcript

25. Animal mo

26. Dysregulatiurrence-free s

27. An outbreaum paratuberculo

28. L-histidine

29. Mucosal dial microbiota


Diseases in 2

proteomic anaession of galec

nction permitsween plants an

irus shedding iome

ated and voltavirus NSP4-mlcium stores

nsiderations font Clostridium d

stics of mucos

L. reuteri derive models

ly-altered lympnduced acute c

mall vessel dis

hibits colorecttional activity

odel of irinotec

ion of purinerurvival in pati

ak of IBD prolosis in the etio

metabolism b

isease activity transplantatio


alysis of esophctin-3

s the transmisnd consumers

duration is as

age-activated cmediated virop

or fecal microbdifficile infectio

sal and fecal m

ved histamine

phatic functiocolitis

ease, obstruct

tal cancer cell through prot

can-induced f

rgic signaling iients with hep

ovides new eviology of Crohn

by Lactobacillus

may predict thon in pediatric

um:

hageal eosinop

sion of geneti

ssociated with

calcium channporin activity t

biota transplaon

microbiota in h

on IL-8 expre

on in mice with

tive sleep apne

growth by regein-protein in

fatty liver disea

is associated wpatocellular ca

idence for a ron's disease

s reuteri

herapeutic resc ulcerative col

philia reveals

ic

stability of

nels are through

ntation in

healthy

ession using

h dextran-

ea, and gut

gulating β-nteraction

ase

with poor arcinoma

ole of M.

sponse to litis

Page:

36.

37.

38.

39. J

40.

41. J

42.

43.

44.

45.

46.

47.

Tex 6th Fron

Name and InLaura Ortiz Graduate StuBaylor CollegMuralidhar PrAssistant ProTexas ChildreCana Ross, PhPostdoctoral Baylor CollegJeremy SchaeAssistant ProUT Health ScTattym E ShaSenior ScientiBaylor CollegJennifer K. SpInstructor Baylor Colleg

Yuxiang Sun,Assistant ProBaylor Colleg

Mary ElizabetFellow Baylor CollegCatherine ToPostdoctoral Baylor Colleg

Hongtao “AleGI Fellow Baylor Colleg

Yong Ma Research AssDepartment oPharmaceuticCollege of Ph

Yuying Liu, PAssistant ProUT Health Sc


nstitution:

dent ge of Medicineremkumar, Mfessor en’s Hospital h.D. Associate

ge of Medicinefer, Ph.D. fessor cience Center aiken, Ph.D. ist

ge of Medicinepinler, Ph.D.

ge of Medicine

M.D., Ph.D. fessor

ge of Medicine

th Tessier, M.

ge of Medicinemaro-DuchesResearch Ass

ge of Medicine

ex” Wang, M.

ge of Medicine

istant of Pharmacolocal Sciences harmacy, Univ

Ph.D., M.Ed. fessor cience Center


nflammator

e MBBS, MRCPC

e

e

e

e

.D.

e sneau, Ph.D. ociate e

D., Ph.D.

e

ogical and

versity of Hou


6

Abstra

P-30. Ldeliver

CH P-31. Idecrea

P-32. Tdifficile

P-33. Einflamm

P-34. Ccells

P-35. Rmecha

P-36. Acorn syinsulin

P-37. Oprotec

P-38. Ifrom L

P-39. Hdeveloepithel

uston

P-40. PPGE2 (TNBS

P-41. Fand syScurfy


Diseases in 2

act Title:

Lactobacillus reury of antimicro

Infants with shased intestinal

The role of GAinfection

Epigenetic andmation in IL-

Characterizatio

Reuterin – Invanism in gut-m

Ablation of ghyrup (HFCS)-

n resistance

Obeticholic action against C

Induction of gL cells by hum

HGF and Metopment, the pelial proliferatio

Perfusion withproduction in

S)-treated rat c

Feeding Lactobstemic anti-in

y mice


uteri as a biothobial peptides

hort bowel sybacterial richn

GABA in susce

d transcription10-/- mouse

on of the peri

vestigation of microbial healt

hrelin receptor-induced adipo

cid (INT-747)Clostridium diffic

glucagon-like pman microbial

t support moueristaltic respoon in response

h celecoxib den 2,4,6-trinitrocolon

bacillus reuteri Dnflammatory e

um:

herapeutic systs.

yndrome (SBS)ness and diver

eptibility to Cl

nal regulation

inucleus in col

a novel signalth

r attenuates hiose inflammat

) confers diseacile infection

peptide-1 prostrains

use enteric neronse, and intese to injury

ecelerates the robenzenesulfo

DSM 17938 pffects in Treg-

tem for the

) have rsity

lostridium

of

lon cancer

ling

igh fructose tion and

ase

duction

rvous system stinal

rates of onic acid

roduces local -deficient

*Weizhen

*DivisionMedicine

Necrotizingmost feareinclude inPathogeneinflammatoOther than Surfactant dampens Tµg/day) sigmodel of Nto demonsSP-A in espurified SPcould be us Rat pups ExperimenVarious amdictated. Omeasure o Unlike prehypoxia treHowever, cof SP-A waWhen ≥5 µwas not odecrease iresults; theconcurrentadministrator IL-1β leameliorateopportunitybeneficial e These resuNEC in its

Tex 6th Fron

Amn Bi, †Nicole

n of Neonatae, #Pediatric

g enterocolited complicangestion of esis of NEory cytokines surgery, eff

protein A (TLR4 activitygnificantly d

NEC. SP-A astrate a dosestablished inP-A that is msed therape

(3 day oldntal NEC wamounts of SOn the fourthof inflammato

viously usedeatment of pchanges elicas administeµg of SP-A observed. ntestinal IL-

e incidence otly with treattion of SP-Aevels. Thes NEC, the y to adminiseffects of SP

ults suggest initial stages


elioration oY. Fatheree

al-Perinatal MResearch C

tis (NEC) resations amon

infant formC involves s and enhanfective treatm

(SP-A) playsy and binds

decreased malso reducede-effect relatntestinal infl

most effectiveutically in es

d) were seas induced bP-A was adh day, pups ory cytokines

d regimes topups did not cited by admered daily, liwas adminiOn the oth-1β levels. of NEC was tment to ind

A 2 days aftese results seffect of SPter SP-A to

P-A are not o

that in addits.


nflammator

of Experimee, †#Yuying LMichael andMedicine, †Denter, DepaSchool at H

sults in the dng prematurmula, intes

exposure nced activityments after o

s a key roleLPS. We h

mortality andd intestinal Ttionship betwammation ine in ameliorstablished N

parated froby thrice dadministered i

were sacrifs by ELISA.

o induce exresult in rob

ministering vattle effect onistered, NECer hand, SDelayed adreduced as uce NEC or

er treatment suggest thaP-A is not reduce NECobserved in

tion to its pr


7

ental NEC byLiu, §Constand *#Joseph LDivision of Grtment of Peouston, Hou

destruction orely-born infstinal hypox

to lipopolyy of toll-like onset of NEC

e in innate have reported the incideTLR4 and inween SP-A n the moderation of NECEC.

m dams, sily exposurein the formuiced and ileu

xperimental bust assessmarious amoun assessmeC was decreP-A appeardministrationwere the lev

r 1 day afterto induce Nt while a thdose-depen

C in the initiaadvanced st

rophylactic u


Diseases in 2

y Surfactannce L. AtkinsL. Alcorn

Gastroenteroediatrics Theuston TX

of all or part fants. Riskxia, and inysaccharide receptor 4 C are lackin

immunity; Sed that gavaence of NECnflammatory and NEC anl. These reC and deter

separated ine to 10 min ula during thum harveste

NEC in thisment of NECunts of SP-Ant of NEC aeased; howered to haven of SP-A (5vels of IL-1βr the initial tEC had littlehreshold levndent. In aal stages of tages of dist

use, SP-A ca


nt Protein-As, #Sam C. F

logy, §Divisioe University

of the bowek factors fontestinal m

(LPS), inc(TLR4) in pg.

SP-A modulage of purifieC in an expcytokine lev

nd to determesults may drmine if adm

nto groups of hypoxia

he initial dailed for asses

s model, resC compared A were obseand IL-1β levever, a dosee a dose-de5 µg) providβ when SP-Atreatment. Oe effect on avel of SP-A ddition, thegastric distrtress.

an be used t

um:

A Flanders, #A

on of Pulmoof Texas Me

el, and is oner developingucosa immcreased levremature int

ates inflammed human Sperimental rvels. Our gomine the efficdefine the d

ministration o

and fed fo(5% O2, 95

ly feeding ossment of NE

sults indicateto untreatedrved. Whenvels was obse-dependenependent efed very inte

A was adminOn the othessessment o

A must be ure is a win

ress. Howev

to ameliorate

len K.

onary edical

e of the g NEC

maturity. vels of testine.

mation, SP-A (5 rat pup oal was cacy of dose of of SP-A

ormula. 5% N2). or when EC and

ed that d pups. n <5 µg served. t effect ffect to eresting nistered r hand, of NEC used to dow of ver, the

e acute

Lacto

Baokun HeDepartmen3Pediatric RHouston, T

Backgrourole in muarthritis (Rattractive tretinoic-acdifferentiatTherefore, inflammatoprobiotic Linflammatio(NEC), andin inflammain inflammthrough suAims: ToRORγ. Methods: were incub(ratio of 1:CD4 and dependentRORα anddomain (LBand IL-17Adetermine genes, inclby real-timResults: Wof IL17A-pincreased containing treatment differentiatWe observdependentoverexpresConclusioRORα/γ ac

Tex 6th Fron

bacillus reu

e1,3, Yuying Lnt of PediatriResearch CeTX 77030, U

nd: CD4+T ultiple inflamRA), and sys

target for thid-receptor-rion of naïvan attractiv

ory diseasesLactobacilluson: lipopold Foxp3+regatory diseas

matory diseappressing thdetermine

For TH17 dbated for 5d1 (LR: cell)intracellular t reporter asd RORγ, in BD) of mousA promoter

the effect oluding IL17Ae PCR.

We found thaproducing Ccompared anti-CD3/C

significantlyion assay. Sved that LRt manner. ssing RORα ons: Probioctivity. LR17


uteri DSM 1

Liu1,3, Thomics, Divisionenter, UniveSA

helper lympmmatory disestemic lupusherapeutic arelated orphve CD4+T cve strategy fs is to inhibs reuteri DSysaccharideulatory T (T

ses remains ases may bhe activities if LR17938

ifferentiation in TH17 ce), re-stimulaIL-17A to

ssay was uswhich the

se RORα or reporter conof LR17938 A, IL17F and

at LR17938 CD4+T cellsto TH0 in w

CD28 but wy decreasedSubsequentlR17938 inhLR17938 aor RORγ, w

otic LR17938938 may be


nflammator

7938 supprrecep

as K. Hoangs of 1Gastro

ersity of Texa

phocytes thaeases, inclus erythematoapplication ahan receptorcells into Tfor the deveit the activit

SM17938 (Le (LPS)-induTreg)-deficien

unclear. Webe partially of RORα ansuppresses

n, naïve CDll differentiat

ated by PMAbe analyzeded to identifDNA bindinRORγ. We

nstruct with on IL-17A

d other RORα

inhibited ms (TH17) in which when

without the d the percely, we assesibited RORalso strongwhich was co8 suppressehelpful in tr


8

resses TH17ptor RORα/

g1,3, Dat Q. Tenterology aas Health Sc

t express intuding inflamosus (SLE). aimed at inrs α (RORαH17 cells, alopment of nty of RORα LR17938) hauced intestinnt Scurfy mie hypothesizdependent

nd RORγ. TH17 cell d

4+T cells isotion medium

A/inomycin wd by flow cfy the effectsg domain oalso co-tranRORα/γ respromoter acα/γ target ge

ouse TH17 cTH17 cell

n naïve CDcomponents

entage of ILssed the effe

Rα or RORγly inhibited

onfirmed by es TH17 celeating TH17-


Diseases in 2

7 cell differe/γ

Tran2,3, and Jand 2Allergy/cience Cente

terleukin-17 matory bowThe discov

nhibiting theα) and γ (ROand for indnovel therapand RORγ

ave been snal inflammce. How LRzed that theon inhibitio

differentiation

olated from m in the preswith brefeldicytometry. As of LR1793

of GAL4 wansfected mosponse elemctivity. The enes, in EL4

cell differentdifferentiatio

D4+T cells ws for TH17 L17A-produfect of LR17γ-dependent IL-17 proreal-time PCl differentiat-mediated in


entiation thr

J. Marc Rho/Immunologer at Housto

(TH17 cells)wel disease very of TH17e function oORγ) are re

duction of Ipeutics to tr. Anti-inflam

shown in 3 mation necroR17938 affece beneficial eon of TH17

n through ta

the spleen sence or abn for 5h, an

A cell-based38 on transcas fused to use RORα o

ment (ROREexpression

4 and TH17 c

tiation in vitron medium

were stimulacell differe

cing TH17 7938 on trant reporter aomoter activCR assays. tion and funnflammatory

um:

rough orph

oads1,3 y/Rheumato

on Medical S

) play a path(IBD), rheu

7 cells provif these cellequired for L-17 transceat TH17-memmatory effanimal mod

otizing entercts TH17 reseffects of LRcell differe

argeting ROR

of C57BL/6bsence of LRnd then staid RORα or criptional actthe ligand

or RORγ fullE) into EL4 c

of TH17 sigcells was qua

ro. The percm was signiated in a mentiation. LRcells in the

nscriptional aactivity in avity in EL4

nction via iny diseases.

an

ology, School,

hogenic umatoid des an ls. The the full

cription. ediated fects of dels of rocolitis ponses R17938 ntiation

Rα and

6J mice R17938 ned for RORγ-tivity of binding l length cells to gnature antified

centage ficantly

medium R17938 e TH17 activity.

a dose-4 cells

hibiting

The assocnormal intKristin N. B1Graduate OH; 2DepaTX. Backgrouin the crypconfined tpopulationspreviously and for steKRAS andallele amevitro cell cuhypothesizhomeostas Methods: inducible recombinaadministereanalyzed Functional jejunal cryp Results: Icoincided wshowed thExpressionrecombinecounterparformation. confirmed Conclusiodownstreanecessary restore norstudy suggdate it is intestine, btheir integrthe specifipathways w

Tex 6th Fron

ciation of Krtestinal proBell1 and NoProgram in

artment of M

nd and Aimpts of Lieberto proliferats is essentshown that

em cell mad HRAS mutliorates the tulture studie

ze that MAPsis.

To determiKlf5-floxed tion of Klf5 ed for five using convstem cell as

pts.

In addition with a loss hat increasn of KRAS ind Klf5 cryprts. Under

However, that stem ce

ons: Data gam of Klf5. for stem ce

rmal progengest a role funclear wha

but given therative naturec regulatorywithin the int


rüpple-like liferation. ah Shroyer1

Molecular aedicine - Div

ms: In the adkühn. Withinting cells. Htial to suppt Klf5 is reqintenance; htations play tumorigenic

es suggest tPK signaling

ne if Klf5 reallele was

and activaticonsecutive

ventional imssays were

to decreaseof phosphoed Klf5 lean vivo, rescupts failed to

these samthese ente

ell loss was m

athered from However

ell maintenannitor proliferafor Klf5 in dat the mecheir known roe in normal y effects of testine.


nflammator

factor 5 and

, 2 and Developmvision of Gas

dult intestinen the intestinHomeostaticport the rapuired for cehowever, tha known oeffects of thhat Klf5 is ris required

equires MAPs combined on of KRAS

e days priormmunohistocconducted in

ed proliferatrylated MEKad to miseued the losso from thee conditions

eroids eventmaintained a

m our rescur, results frnce and noration rather tifferential sihanism of Kole intestinal

homeostasiKlf5 and ho


9

d mitogen-a

mental Biolostroenterolog

, all proliferanal crypts exc maintenanpid turnoverellular prolifee mechanisncogenic ro

his signalingrequired for for Klf5’s p

PK signalingwith cons

S were driver to sacrificchemistry, n vitro using

tion within K and ERK.expression s of proliferae characteriss, reexpresstually die liafter reexpre

e experimerom these rmal proliferathan stem cgnaling path

Klf5 or the disease, sp

is. Future eow this may


Diseases in 2

activated pr

ogy, Universgy, Baylor C

ative stem axpression ofnce of thesr of the interation to msm by whichole in intestig pathway inMAPK signaproproliferati

g for prolifestitutively aen by Villin-cce on the swestern bl

g three-dime

the crypts Converselyand increa

ation. Additistic buddingsion of KRAke those Kession of KR

nts suggestexperiments

ration, MAPKcell numbershways for strole of MAP

pecifically caexperimentsy integrate


rotein kinas

sity of CincinCollege of Me

and progenitof the transcrse stem antestinal epit

maintain inteh this worksnal cancers this contexaling. Givenive nature i

eration withinactive KRAScreER in micsubsequent ot analysis

ensional ente

of the intesy, immunohase of phoonally, enteg structure AS was ab

Klf5 KO enteRAS in these

t that MAPKs indicate, K signaling is. Preliminatem and proPK signalingancer, it is ims will be reqwith other k

um:

se signaling

nati, Cincinnedicine, Hou

or cells are ription factornd progenitthelium. Westinal homes remains us. Loss of ont. Furthermn these resun normal in

n the intestS. Simultace. Tamoxifeday. Tissu

s, and RT-eroids derive

stine, loss istological a

osphorylatederoids isolate

of their wble to rescueroids. RTe mice.

K signaling mthat while is only sufficry results fro

ogenitor cellg is in the mportant to duired to detknown prolif

g in

nati, uston,

located r Klf5 is tor cell e have

eostasis unclear. ne Klf5

more, in ults, we testinal

ine, an aneous en was ue was -qPCR. ed from

of Klf5 analysis ERK.

ed from wildtype ue their T-qPCR

may be Klf5 is cient to om this s. To normal discern termine ferative

Human In

Blutt SE1, SME1,Foulke1. Departm2. DepartmMedicine, BCollege of

A significanpre-clinicalmodels of Clever’s Lastructures,goblet, entagonists. Wmodels of HRVs havesmall animreplicate inrange and

In ordifferentiatbank of Hquantitatedcytometry assay. HRHIEs, conscompared compared compared immunofluoinfected cecauses diachloride chphysiologicinfection asecretion.

Thespathophysinfections pathogen within the prevent/treexamine th

Funding: N(Baylor), a57007689.

Tex 6th Fron

ntestinal En

Saxena K1, Ee-Abel J2, In

ment of Molement of MediBaltimore, MMedicine

nt limitation l models thathe small intab (Hubrech which contteroendocrinWe have chuman rotave been limit

mals. RVs n mice whedo replicate

rder to deteed and und

HIEs (N=52d the (1) amand immuno

RVs infected sisting prima

to fully diffto 37.6%).to undiffe

orescence sells, includingarrhea by sehannel activcal changesand NSP4

e findings iology and tsuch as HRinteractions epithelium i

eat diarrheal he role of the

National Insand P30-DK


teroid Cultu

Ettayebi K1, n J2, Kovbascular Virologcine, Gastro

MD; Correspo

in translatioat recapitulattestinal epithht Institute). tain the nor

ne, and Panharacterizedvirus (HRV) ted as they generally exreas mouse

e in mice. ermine whetdifferentiated) derived fmount of viofluorescencmore cells

arily of immaferentiated H Like HRVerentiated studies valig presence everal mechvity. We invs in HIEs. treatment o

establish Hthe intestinaRV infection

such innaten response disease. In

e microbiota

stitutes of K089502 (H


nflammator

ures: A New

Zeng X1, Brnjuk O2, Zacgy and Microoenterology onding Auth

nal researchte human phhelium usingHuman inte

rmal compleneth cells) ad these newinfection, ware difficult xhibit host r

e RV and so

ther RVs exd HIEs fromfrom patienral RNA byce confocal mwithin HIEs ture enterocHIEs that cV, infectionHIEs (13%dated that of virus facto

hanisms inclvestigated wThrough tim

of HIEs ind

HIEs as newal epithelial rn. HIEs allowe immune rto infection addition, HIin altering in

Health GranHopkins) an


10

w Functiona

roughman J1

chos NC2, Doobiology, BaDivision, Johor: Estes MK

h in the gasthysiology andg advancemestinal enteement of intand are physw, non-transhich kills neto culture in

range restricome other a

xhibit host m several pa

t small intey qRT-PCR, microscopy,than ARV (

cytes and steconsist pred with ARV

% compareHRV-infecteories (viroplauding modu

whether HRme-lapse muced lumin

w models tresponse, inw us to addresponses, s

as well as Es provide anfection or d

nts U18-TRnd Howard


Diseases in 2

al Model of

1, Crawford Sonowitz M2,

aylor Collegehns HopkinsK, Dept. of M

trointestinal d disease pa

ments in stemroids (HIEs)testinal epitsiologically asformed, 3Darly 500,000n transformection in repanimal RVs

range restratients with estine biops (2) numbe and (3) yie(50% compaem cells, weominately owas also

d to 8%)ed HIEs shasms) and iulating fluid RV or the Rmicroscopy, wnal swelling

to understancluding hosdress new stem cell acto identify aa physiologidrug treatme

R000552, RHughes M


Gastrointes

SE1, Karandand Estes M

e of Medicines University SMolViro and

tract is the aathology. W

m cell biolog) self-organithelial cell tyactive base

D HIE cultu0 children aned cell lines

plication. Thu(ARV) exhi

iction in HIeither HRVsies or sur

er of infecteld of virus byared to 13%

ere less suscof mature ehigher in d. Electron ow classicanduction of flow throug

RV enterotowe observeindicative

and host phst restrictionquestions activity, cell-cand test newically relevanent.

R01-AI08065Medical Res

um:

stinal Virus

dikar U1, ConMK1

e, Houston, School of Micro, Baylo

absence of e have estay pioneeredize into villuypes (enterd on responres as pre-nnually. Studs and do nous, HRV doibit a broade

Es, we inocs or ARVs rgical tissueed cells usiny fluorescen

%). Undiffereceptible to in

enterocytes differentiated

microscopal features lipid dropleth increased

oxin, NSP4, ed that bothof increase

hysiology, d to gastroin

about humancell communw drug therant model sys

6, P30-DK0search Fell

s Infection

nner

TX

or

reliable blished

d by the us-crypt rocytes, nses to -clinical dies on

ot infect oes not er host

culated from a

es. We ng flow nt focus entiated nfection (12.6% d HIEs y and of RV-s. HRV

d apical cause

h HRV ed fluid

disease testinal n host-nication apies to stem to

056338 owship

Min-Shan C 1. IntegrativHouston, TCollege of Colorectal the Unitedrepressor iintestinal ecancer, suunknown. that the geGfi1 has a suppressoGfi1 stainiexpressionfocus on econditionalexpressionFuture stuunderstand

Tex 6th Fron

Gfi1 func

Chen1, Noah

ve MolecularTexas, USA,Medicine, H

cancer (CRd States. Thimplicated inepithelium. uch as leukRecent genoene express

role in tumor of CRC tuing comparen of Gfi1 in examining tl deletion of

n of Gfi1 in iudies for ideding of tumo


tions as a p

h F Shroyer1

r and Biome 2. Division o

Houston, Tex

RC) is the thhe growth fn the differenPrevious stu

kemia and nome-wide as

sion of Gfi1 or developmumorgenesised to normhuman colothe role of Gfi1 in intes

intestinal tumentifying theor progressio


nflammator

potential tumin colore

1,2

edical Sciencof Medicine, xas, USA

ird most comfactor-indepentiation of seudies suggeneutropeniassociation stis associate

ment in CRCs. In our wo

mal tissue inorectal cells Gfi1 in CR

stinal epithemor may pree molecular on and benef


11

mor supprectal cancer

ces GraduateSection of G

mmon and tendent 1 (Gecretory precested that g. However, tudies from

ed with less . Therefore, rk, we find

n human coresults in in

RC in ApcMin

lium will resevent tumorfunction of

fit to therape


Diseases in 2

essor by indr cells

e Program, Gastroentero

the third leaGfi1) zinc ficursors into gain or loss

the role ofThe Cancertumor aggr we hypothethat maligna

olorectal spncreased apn mouse m

sults in worsrgenesis andf Gfi1 in CReutic strateg


ducing apop

Baylor Colleology & Hep

ading cause inger is a t goblet and

s of functionf Gfi1 in Cr Genome Aressiveness esize that Gant CRC ce

pecimens. Mpoptosis. Fuodel in vivoe outcome. d prolong ovRC may imies.

um:

ptosis

ege of Medicpatology, Bay

of cancer dtranscriptionPaneth cellsn of Gfi1 le

CRC is still Atlas have re

in CRC, indfi1 acts as a

ells display wMoreover, trauture directioo. We expeIn the contr

verall survivmprove our

cine, ylor

death in n factor s in the eads to

largely evealed dicating a tumor weaker ansient ons will ect that rast, re-val rate. current

Ka Liu1, Ya1Deparmen

Backgroumorphogenpancreatitissuggest thhypothesizCP. Objective:Methods: (BMPR2+/-)TGF-β1 (1measuringmatrix protResults: IGremlin (1FN, BMP2 treatment Gremlin alBMPR2+/- PConclusioBMPR2 is novel medrepression

Tex 6th Fron

anna Cao1,2,

nt of Surgery

nd: Our labnetic proteis (CP). Deat Gremlin i

ze that Grem

: Determine PSCs were

). The cultur ng/ml), or v phospho(ptein, was men wt PSCs2.5- vs 2.9-inhibited TGof TGF-β, lone inducePSCs (p<0.0ons: Gremlin

required fordiator of pan of BMP sign


A Nov

George H.

y, UTHSC-H

boratory hasn (BMP) a

eletion of Gs pro-fibroge

mlin blocks t

the role of Be isolated fred PSCs wvarious com

p)Smad1/5 leasured by im, comparedfold with theGF-β’s effecBMP2+TGF

ed FN by 205). n promotes r Gremlin’s pncreatic fibronaling, leadi


nflammator

vel Mediator

Greeley, Jr2

H; 2UTMB, TX

s shown thaantagonist, Gremlin in m

enic in CP. he anti-fibro

BMP signalinfrom wild-ty

were treated mbined treatm

evel using mmunofluore to vehicle,

e treatment ct, and GremF-β, Gremlin.3-fold in w

pancreatic pro-fibrogenosis in CP. ng to an inn


12

r of Chronic

2 and Tien C

X

t pancreaticare elevate

mice attenuaHowever, th

ogenic BMP

ng in Gremlinype (wt) an

with vehiclements. ActivWestern blescence as , BMP2 indof BMP2 vs

mlin blocked n+BMP2+TG

wt PSCs an

fibrosis throic function. TStrategies tovative CP t


Diseases in 2

c Pancreatit

C. Ko1,2

c levels of Ged in both ates CP-ind

he underlyinsignaling, le

n-induced pnd BMP rece, Gremlin (vation of BMotting. Fibroa functionaluced pSma

s Gremlin+BBMP2’s effe

GF-β respecd this effec

ough its bloTogether, wto target patherapy.


tis

Gremlin, an human an

duced fibrosg mechaniseading to pa

ancreatic fibceptor type (500 ng/ml), MP signalingonectin (FN outcome of

ad1/5, whichMP2, p<0.0ect (4.7-, 1.2ctively, p<0ct was atten

ockade of Bwe have idenancreatic Gre

um:

endogenound mouse csis. These m is unknow

ancreatic fibr

brosis. II knockouBMP2 (50

g was assesN), an extraf fibrosis. h was inhib05). TGF-β in2-, 4.8-fold w.05). Furthenuated by 7

BMP signalinntified Gremlemlin may r

s bone chronic results

wn. We rosis in

ut mice ng/ml),

ssed by cellular

ited by nduced with the ermore, 78% in

ng and lin as a release

Stoo

J.L. Cope (M.M. Tham1. DepartmTexas ChilHouston, TChildren’s Houston, TIndies, Mo

Despite ad(LBW) babincrease aassociationcases, redincreased cTo investigutilization aTheir stooincluding toarginine m16S rRNA the OTU asubjects. Three domcharacterizClostridiumsamples, babsorptive abundanceendogenoulikely to hatotal carboor the mixweight, higwith physiodetected asuggest thdominant cin the PLachnospir We demonpotential torepresent arisk for LBW

Tex 6th Fron

ol microbio

(1,2), J.W. Hme (5), A.V. ment of Patho

dren’s MicroTexas, USA;Nutrition Re

TX, USA; 4. na, Kingston

dequate dietabies at high rarginine pron between tduced bioavacatabolism bgate whetheand metaboll microbial otal carbohy

metabolic patgene from s

assignments

minant comzed by increm, respectivebut not exclu

capacity anes of Clostus arginine fave a Bacterohydrate intaxed Bacterogher energy ological meaamong the mhat the convcommunitiesPrevotella-doraceae and

nstrate that to impact arga future treaW babies.


me composmetabolis

Hsu (3), P. DKurpad (4), ology and Imobiome Cent 3. United S

esearch CenSt. John’s Rn, Jamaica

ary intakes orates. Previo

oduction durthe prevalenailability of by arginase,er the gut clism from Amcommunities

ydrate and ethways. 454stool. Sequewere used

mmunity typeased abunely. These d

usively so. Snd a lower tridium showflux. Subjectroides-dominake possiblyoides with C

and total caasurements members ofversion of as. Likewise, ominated cRuminococc

the gut micrginine availa

atment for in


nflammator

sition and psm in a mul

Dwarkanath (J. Versalovi

mmunology, ter, Departmtates Departer, Departm

Research Ins

of energy anous researchring pregnance of LBWarginine wa possibly byommunities

merican and s, dietary hnergy intake

4 pyrosequeences were to generate

pes were indances of dominant stubjects harbendogenous

wed a mars with greate

nated commy due to highClostridium-darbohydrate

of argininef this multi-narginine to the further c

communitiescaceae.

obiota vary ability in theadequate ar


13

predicted futi-national c(4), J. M. Kac (1), E.B. HBaylor Colle

ment of Pathortment of Agrment of Pedistitute, Bang

nd protein, Inh has shownncy, Indian

W babies anas not due ty the gut mic

of Indian wJamaican w

abits, and mes, gut absoncing was uassigned to

e functional p

identified agenera Pretates tendedboring Prevos arginine fked increaser body weigunity even w

h gut absorpdominant typ

intake, and flux and thnational cohornithine is

conversion os as they

in conjunctioe human horginine avail


Diseases in 2

unction reflecohort of w

arnes (3), C.CHollister (1,2ege of Medicology, Texasriculture, Agatrics, Bayloalore, India;

ndian women that, althou

women dond reduced to inadequatcrobiota. women diffewe recruited metabolic ch

orptive capacused to seqo operationapredictions,

among the votella, Bacd to reflect otella-dominaflux, while cse in both ght and gut awith a conveptive capacitpe occurredlower gut a

he three domhort, predicts likely to bof ornithine ty largely

on with argiost. Modulatiability during


ect differentwomen

C. Kao (3), R), F. Jahoor cine, Houstos Children’s

gricultural Reor College of 5. Universit

en give birth ugh women o not, and arginine prte dietary in

er in composa multi-natio

haracteristiccity, and theuence the V

al taxonomic which were

stool speccteroides, othe geograpant communcommunities

gut absorpabsorptive c

erse low enety values. P

d in subjectabsorptive caminant fecaions of met

be higher into citruline islack the

nine metaboion of the gg pregnancy

um:

tial arginine

R.A. Luna (1(3)

on, Texas, UHospital,

esearch Statf Medicine, ty of the We

to low birth from other nthere is a

roduction. Inntake but ra

sition and aonal cohort

cs were evae kinetics of sV3V5 region

units (OTUe compared

cimens andr Bacteroidephic origin onities had lows containing ptive capacicapacity werergy intake aPrevotella-dos with loweapacity. Conl communitytagenomic fun the Bactes likely to beFirmicute

olism and hagut microbioy and decrea

e

1,2),

USA; 2.

tion,

st

weight nations strong

n these ather to

arginine (n=27).

aluated, several

n of the s), and among

d were es with of their wer gut higher

ity and re more and low ominant er body ngruent y types unction

eroides-e lower genera

ave the ta may ase the

Impaire

Jeanette CBaylor Col Rotavirus requires thdroplets (Lhours postMature LDintracellulais unknown We recentdispersed appears aNSP5: dNSwith hypeviroplasm frequiremen

We evaluabecause ehyper-phosprior to infInfectious CKI/CKII-insize, impaidemonstra

Our resultsmay lead to

Tex 6th Fron

ed rotaviruspr

Criglar, Sue Clege of Med

(RV) replicahe interactioLDs). RV inf infection (h

D/viroplasmsar membranen.

ly reported tform of NSt ~3 hpi. EaSP2 only asser-phosphoryformation. Snt for cellula

ated the roleeach kinase sphorylationfection and ayield was d

nhibited cellired lipid dro

ated a decrea

s suggest tho the discov


s viroplasmrovides new

Crawford, anicine, Houst

ation occurson of RV nofection indupi). LD/Virop

s enclose thes containin

that two formSP2 (dNSP2ach form ofsociates withylated NSP

Since no RV-r protein kin

s of casein has been im. Cells wereassayed by determined bs showed a

oplet associaase in NSP5

hat both CKIvery of a new


nflammator

formation w clues into

nd Mary Esteon, TX. 7703

s in cytoplasonstructural ces LD formplasms increhe viral geng RV nonstr

ms of NSP2) appears af NSP2 inteh hypo-phos

P5, suggest-encoded proases in RV

kinase I (CKmplicated ine pre-treateimmunofluo

by fluorescea delay in viation, and litt5 hyper-phos

and CKII hw phosphory


14

and maturao cellular lip

es. Departm30

smic inclusiproteins NS

mation and ease in size nome replicaructural prot

2 are producat ~2 hpi, aeracts differesphorylated ting a phootein kinasereplication u

KI) and casen NSP5 phod with inhib

orescence ment focus asroplasm formtle or no asssphorylation

ave a role inylation-depen


Diseases in 2

ation in protpid droplet f

ment of Molec

ions, called SP2 and NSnascent virointo larger, mation machtein NSP4. H

ced during Rand a viroplaentially with NSP5 while

osphorylatione has yet beeusing target-

ein kinase IIosphorylationbitors to onemicroscopy (ssay. IF demmation, dramsociation wit.

n viroplasm ndent mecha


tein kinase-formation

cular Virolog

viroplasmsSP5 and cooplasms formature viropinery and aHow RV ind

RV infectionasm-associa specific ph vNSP2 assn-dependenen describedspecific inhi

(CKII) on vn and NSP2e or both ki(IF) and wesmonstrated matically deh NSP4. We

growth andanism of viro

um:

-inhibited c

gy & Microbi

, whose foromponents rm on LDs aplasms by ~5are surroundduces LD for

. A cytoplasated form (vhospho-isofosociates exclnt mechanisd, we assessbitors.

viroplasm for2-dependentinases (or vstern blot anthat viropla

ecreased viroestern blot a

d maturationoplasm asse

cells

ology,

rmation of lipid at ~2-3 5-6 hpi. ded by rmation

smically vNSP2) orms of lusively sm for sed the

rmation t NSP5 vehicle) nalysis.

asms in oplasm

analysis

, which embly.

The mic

Carolina G1Skirball InDepartmenMedical Insand MicrobMedicine, H

The intmaintainingmicrobiotasystem andpathologicaunderlie thsame immdysregulatto pathoge

In orde

limiting intemononucleand efficienwell as in mwith evidenCX3CR1+ Mmucosal heintestine toresponsesfunction anWe hypothhomeostasdysregulate

To stud

MNPs can in modulatidentify CXresponseslimiting inflpresentatioconditions inflammatomicrobiotainflammatomay promoUnderstandintestinal in

Tex 6th Fron

crobiota con

Galan1, Randnstitute, NYUnt of Medicinstitute, NYUbiome ReseaHouston, TX

testinal immug a symbioti). A growingd the microbal inflammate developmunostimulatoion, a critica

ens while avo

er to prevent estinal inflamear phagocytnt at killing inmouse colitisnce of both pMNPs integrealing. First,o the mesent. Second, si

nd repair bothesize that Csis by limitinged in IBD.

dy the in vivobe selectiveing T cell res

X3CR1+ MNP. They are cammatory im

on by CX3CRwhere the m

ory T cell res, CX3CR1+ c

ory T cell resote inflammading this regnflammation


nditions CX

dy S. LongmaU School of Mne, Weill-Cor School of March and MoX, USA

une system c relationsh

g body of evibiota are esstion against ent of inflamory molecule

al question isoiding inflam

and treat IBmmation. Onte (MNP). Cntracellular bs models, bupro- and antrate signals f, recognitionteric lymph ngnals from tth in mice an

CX3CR1+ cellg inflammati

o role of thesely depletedsponses to i

Ps as critical critical both fommune respR1+ cells is cmicrobiota hasponses. Togcells are critisponses. Disatory behavigulation of C and the trea


nflammator

X3CR1+ monresponses

an2, Dan R LMedicine, Nernell Medica

Medicine, Neolecular Viro

must protecip with an endence demo

sential for huthe microbio

mmatory bowes as pathogs how the intmmatory resp

BD, we must ne critical inteX3CR1+ MNbacteria. Thut their role ii-inflammatofrom the mic

n of the micronode. We hyhe microbiot

nd humans tls respond toion and prom

se cells, we . We used thntestinal antfor limiting tor inducing t

ponses againcritical for pras been pertgether, our fcal for intest

sturbances inor of these c

CX3CR1+ MNatment of IB


15

onuclear phs in the inte

Littman1,3, Gew York, NY

al College, New York, NYlogy & Micro

ct the host fronormous loaonstrates thauman healthota. Breakdowel diseases gens and catestinal immuponses again

first undersestinal cell pPs isolated is populationn the norma

ory behaviorcrobiota to limobiota limits ypothesize thta induce CXhrough the ro microbiotamoting barrie

generated nhese mice totigens. In thethe inductiontolerance to nst pathogeniming these turbed, CX3Cfindings indictinal homeosn the microbcells leadingPs will open

BD.


Diseases in 2

hagocytes testine.

Gretchen E. DY, USA. 2Theew York, NY, USA. 4Alkeobiology Dep

om pathogead of residenat interaction. Thus, a nu

own of these (IBD). As thn trigger influne system nst the micro

tand the celpopulation isfrom humann expands inal intestine ar. We recentlmit intestinaCX3CR1 MN

hat this limitX3CR1+ MNPregulation of

a-derived siger function, a

novel mouseo understande presence n of inflammsoluble prot

ns. We furthT cell respo

CR1+ MNPscate that, in stasis throug

biota, such ag to a loss ofn up new the


to limit infla

Diehl4 e Jill RobertsY 10021. 3Hoek Center forpartment, Ba

nic microorgnt microorgans between tmber of mec

e mechanismhe microbiotammation amounts protobiota.

lular and mos a CX3CR1 n colon are hn the colon oas well as in ly demonstra

al inflammatioNP migrations microbiotaPs to promof innate lymp

gnals to mainand that thes

e strains, in wd the role CXof the intact atory intestitein antigenser demonstr

onses in vivos promote the

the presencgh promotio

as those thatf intestinal hoerapeutic tar

um:

ammatory T

s Center for oward Hughr Metagenomaylor College

ganisms whinisms (the the immunechanisms lim

ms is thoughta displays th

and disease tective respo

olecular procexpressing

highly phagoof IBD patienIBD is uncleated two waon and promn from the

a directed T ote mucosal phoid cells (ntain intestinse pathways

which CX3CX3CR1+ MNPmicrobiota,

nal T cell s as well as rate that anto. In contraste induction oce of the intan of anti-t occur durinomeostasis.rgets for limit

T cell

IBD, hes mics e of

le

mit t to he upon onses

cesses

ocytic nts as ear, ays mote

cell barrier ILCs).

nal s are

R1+ Ps play we

igen t, in of act

ng IBD ting

The

David J. DRobert Bry1 Dept. of AChildren’s USA. Obstructivesleep, is a States. OSmost commhypertensiopathologicaWe hypotinflammatby chronicaremotely ccycle in freon a normrats (underwhen rats in systolic p<0.05) of(ampicillin p<0.05), Oin the gut mFecal samevaluate thsignificant (48% vs. 4hypertensiointo normodeveloped a key role f

Tex 6th Fron

e role of the

urgan, PhD1

yan Jr, PhD1

AnesthesioloMicrobiome

e sleep apnsignificant c

SA has beenmon underlyon is likelyal cascade. hesized tha

tion and ultally implantiontrolled by ee-ranging raal chow dierwent surgewere fed a hblood press

f apneas. Inand neomy

OSA-inducedmicrobiome ples from no

he microbiomincrease in

4%; n=4-6, pon we transotensive OS

hypertensiofor the gut m


gut microb

1, Eric E. Llo.

ogy, 2 Dept. oCenter, Dep

nea (OSA), clinical probln shown to bying cause

y multifactorThe source at alterationimately hypng an inflataa computer

ats. We havt do not devry without ahigh fat diet sure after 1nterestingly, ycin), resulti hypertensiofollowing higormal chow me diversity n Firmicutes p<0.05). To splanted cecSA rats that on within 7 dmicrobiome i


nflammator

biome in ob

oyd, PhD1, E

of Pathologypartment of

characterizem affectingbe an indepof resistant

rial, inflammof the inflam

ns to the gpertension.able obstrucr to produce ve previouslyvelop hypertpneas) fed afor 3 weeks (19mmHg; when rats fng in a sig

on was abolgh fat diet, wand high faand compos(49% vs. 8

further demcal contents

had been days of OSA n the develo


16

bstructive sl

mily B. Holli

and ImmunPathology, T

ed by repeg upwards ofpendent risk t hypertensio

mation is commation assgut microbiAirway obsttion device (60 apneas/

y demonstratension folloa high fat dis prior to apn

n=10-13, pfed a high nificant decished. Thesewhich may bat diet rats wsition. Comp81%; n=4-6onstrate theisolated fro

previously tA (n=4, p<0.0opment of O


Diseases in 2

leep apnea

ster, PhD2,3,

nology, BayloTexas Childr

ated closuref 25% of thefactor for sy

on. While onsidered asociated witiome durintructions, sim(OD) in the /hr (10 sec. eated that youowing 4 weeet do not deneas, they e

p<0.05) and fat diet wer

crease in Fie observatio

be required fwere sequenpared to nor, p<0.05) ae importanceom hypertentreated with 05). In conclSA-induced


induced hy

, Julia L. Co

or College ofren’s Hospita

e of the upe adult popuystemic hypthe etiology

an integral h OSA is nog OSA pro

mulating apntrachea of raeach) duringung healthy

eks of OSA. evelop hypeexhibited a s

2 weeks (2re treated wirmicutes (8ons led us tofor OSA-indunced for the mal chow, hnd decreasee of dysbiossive OSA raoral antibio

usion, these hypertensio

um:

ypertension

pe, PhD2,3, a

f Medicine, 3

al, Houston,

pper airway lation in the

pertension, ay of OSA -incomponent

ot presently oduces low neas, were inats. The ODg 8 hrs of therats (8 weeAdditionallyrtension. Ho

significant ele21mmHg; n=with oral ant1% to 2%,

o examine chuced hyperte16s rRNA g

high fat diet le in Bactero

sis in OSA-inats on high otic. Recipiee data demoon.

n

and

3Texas TX,

during United

and the nduced in the

known. grade

nduced Ds were e sleep

eks old) y, sham owever, evation =10-11, tibiotics n=3-6,

hanges ension. gene to led to a oidetes nduced fat diet

ent rats onstrate

Melinda En 1. Departm2. Departm Intestinal mand a matrmucin expaberrant exgrowth conwell docummucins. ToMTX-E12 contrast toMUC5ac aClostridiumLactobacillspecies Ctorques, Bbacterial stransmembPeriodic Amonolayerstool mucalterations agents to c

Tex 6th Fron

Human g

ngevik1,2, Be

ment of Pathoment of Patho

mucus, consrix for bacterression andxpression ofnditions durimented, littleo address thwas incuba

o healthy coand contain m coccoides,lus brevis an

C. coccoidesB. bifidobactspecies did brane mucinAcid Schiff- rs. Microbesus, indicatinof MUC5ac

colonic tumo


gut microbi

rkley Luk1,2,

ology & Immology, Texas

isting of glycrial adhesion/or mucin gf mucins withing invasion

e is known ahis gap in knted with 16 olon, which

increased , C. butryicund Bifidobacs, Bacteroidterium and not alter M

ns Muc1, 3 Alcian blue

adhered pong altered c may yield ors of the inte


nflammator

ota alter int

Bhanu Priya

munology, Bas Children's

cosylated mn/colonizatiolycosylation h distinct olig

n and metasabout the intnowledge, th

human gutsecretes M

amounts of um, B. producterium longudes thetaiota

B. infantisMuc2 expreand 4. Chae (PAB-AB)oorly to coatadhesion wnew combinestinal muco


17

testinal mu

a Ganesh1,2

aylor CollegeHospital Ho

ucin proteinson under nor

are associagosaccharid

stasis. Althouteraction of he mucus prt microbiota

MUC2 mucintransmemb

uct, Akkermum induced aomicron, A

decreasedssion. Strainges in muc) stains, thted HT29-M

with alter olnation treatmosa.


Diseases in 2

cus in HT29

, Christina M

e of Medicinouston Texas

s, provides armal homeoated with thede structuresugh tumor-athe gut micrroducing ad species unn, HT29-MTbrane MUC1

mansia mucinrelease of M

A. muciniphi Muc5ac gin-specific acin gene exat detect m

MTX mucus cligosacchariments for en


9-MTX-E12

Mora1,2, Jame

ne s

a protective static condite developms protects tuassociated mrobiota with enocarcinom

nder anaeroTX cell secr1 and MUCniphila, EnteMUC5ac fromila, L. reute

gene expresalterations wxpression wemucin protecompared wde content.

nhanced acc

um:

cells

es Versalovi

barrier for thtions. Alteratent of cancemors from a

mucin changcancer-asso

ma cell line obic conditiorete high le

C3. Incubatioerococcus fam goblet celeri, Ruminossion, whilewere observere correlate

eins of HT2with healthy . Bacterial-scess of thera

c1,2

he host tions in er. The

adverse ges are ociated HT-29-

ons. In vels of on with aecium, lls. The

ococcus e these ved for ed with 29-MTX human specific apeutic

Attenu

Chunxu GaRasik Shah

1Departme2Departme3Departme4Section ofHouston, T Backgrouamelioratinbut the unharboring histamine frole of hista Methods aadministratcolitis wasamyloid Aexpression[18F]fluorostudies shdecarboxydiet and sigsulfate-ind6475 signifin the colohdcA isogesuch anti-csuppressin Conclusiocolitis and findings linmicrobiomecombinatiomicrobiolog

Tex 6th Fron

ation of col

ao1,3, Angelah4, Robert S

ents of Molecents of Pathoent of Patholof GastroenteTX

nd: Suppleng intestinal nderlying ma complete from L-histidamine in alle

and Resultstion of hdc+ indicated b

A protein con of pro-inflodeoxyglucoshowed that lase gene (gnaling via tuced inflamficantly decrn of male Henic mutant carcinogenicng carcinoge

on: These cinflammatio

nk luminal ce and probio

on of diet, pgy.


lonic inflamp

a Major3, BhSteven Fultz3

cular Virologology & Immogy, Texas C

erology and H

ementation inflammatioechanisms hdc gene

dine suppreseviation of in

s: Using a t+ L. reuteri by decreaseoncentrationammatory cse (18F-FDG

suppressio(hdcA) into tthe histaminmation-asso

reased the ndc-/- mice coof L. reuter

c effects, indenesis.

ombined invn-associated

conversion ootic-mediate

probiotic and


nflammator

mmation andprobiotic La

anu Priya G3, Monica Lu

gy & Microbiounology, BaChildren’s HHepatology,

with probion and inflamare unknowcluster whicss TNF prodnflammation.

trinitrobenzestrain 6475d weight los

ns. Mice rcytokine geG) in the co

on of colitisthe intestinae H2 receptoociated coloumber and s

ompared to cri 6475 whicdicating a ro

vestigations d colonic ca

of dietary coed suppressd disease p


18

d inflammatactobacillus

Ganesh3, Susugo3, Vanes

ology, Bayloaylor CollegeHospital, Hou

Departmen

otic Lactobmmation-asswn. Previousch is responduction in ac.

ene sulfonic 5 protected ss, ameliorareceiving Lnes IL-6 anolon by posis dependedal microbiomor. Moreoverectal cancesize of coloncontrol miceh lacks the ole of the h

indicate thaancer via conomponents (ion of colon

phenotype m


Diseases in 2

tion-associs reuteri

san Venablessa Jackson3

or College ofe of Medicineuston, TX nt of Medicin

bacillus strasociated cols studies snsible for thctivated THP

acid-induceBalb/c mice

ation of colo. reuteri 64nd IL-1β, asitron emissiod on introdme, consumer, using an aer model, onic tumors ae that receive

histamine phdcA gene a

at hdc+ L. renversion of L(amino acid

nic inflammamay result in


ated colore

e3, Zhongche3, James Ve

f Medicine, He, Houston,

e, Baylor Co

ains has blonic cancershowed thathe synthesisP-1 cells, ind

ed mouse me from colitonic injury a475 also ss well as ron tomograpuction of a

mption of a hazoxymetharal administnd uptake oed media on

producing acand producti

euteri attenuL-histidine tometabolism

ation and can opportunit

um:

ectal cancer

eng Shi3, Raersalovic1,2,3

Houston, TXTX

ollege of Me

been effectr in rodent mt L. reuteris and secredicating a po

odel of colitis. Suppresnd reduced

showed decreduced uptphy (PET). an intact hhistidine-conane/dextran stration of L. of 18F-FDG bnly. Meanwhctivity did noion of histam

uates expero histamine.

m) by the inncer. The eties for thera

r by

ajesh

X

dicine,

tive at models, strains

etion of otential

tis, oral sion of serum

creased take of Further istidine

ntaining sodium reuteri

by PET hile, the ot show mine in

imental These testinal ffective apeutic

Glucagon

Xuemei Sh

1Children'sMedicine, HUniversity College of

Backgroureprogramcoupled wabout whicadaptationapproved proabsorptpleiotropic and signalprecursorsWe hypothglucose topathway. Tmetabolic modulates Methods: metabolic tracer andinhibitor (3Results: Wfor GLP-2 MS/MS-baaerobic glreprogramidentified tenzyme). G(PKM2, a that GLP-2proliferatiofor couplinfundamentin part by Center.)

Tex 6th Fron

n-like peptid

hi1, Tiago Alv

s Nutrition ReHouston, TXSchool of MMedicine, H

nd: Emergimed for ste

with crypt cech signals dr/regeneratioby the FD

tive, proliferaactions areing in intes

s, while GLPhesized that o support pTo address reprogrammmetabolic rHuman/ mofluxes and c

d BrdU inco-bromopyruv

We show thato augment

ased metabolycolysis anming and cethat GLP2RGLP-2 acutekey isoform

2 plays a novn in the crypng metaboltal aspect of

NIH grant


de-2 reprog

ves2, Xilei Ze

esearch CenX; 2Departmeedicine, New

Houston, TX.

ng evidenceem cell prolill proliferatiorive the metaon. GlucagoDA to treaative, cytopr mediated ttinal epithel

P-2 is secretGLP2R actiroliferation if the nutrie

ming and prreprogrammouse jejunalcell prolifera

orporation. Tvate, 10 µMat a) the GLPt cell prolifeolomics, wend de novoell proliferatio

R was engagely induced

mediating tvel role in mpt stem cellsic reprograf intestinal ad

DK56338,


nflammator

grams gluco

eng3, Richar

nter, Departments of Endow Haven, CT

e suggests feration; anon after Roabolic reprogon-like pept short bo

rotective, anhrough the ium are pooted from villovation in intby triggering

ent-responsivoliferation, wing of glucol crypts weration in the The mini-gu) and labeleP2R was reqration in an

e revealed to biosyntheon were negged in glycphosphorylathe Warburgetabolic reps. Thus, GLPmming anddaptation/ rewhich supp


19

ose metabocells

rd Kibbey2, M

ments of Peocrinology anT; 3Departm

that a) glud b) intestinux-en-Y gasgramming o

ptide-2 (GLwel syndrod anti-inflamdistinct GLPorly definedous enteroeestinal stemg aerobic gve GLP-2 iswe wanted ose and cellre isolated amouse mini

uts were tred with U-13Cquired for th aerobic glythat GLP-2 sis of glutagated by glycolysis via ination and nug effect) in trogrammingP-2 may be

d cell prolifeegenerationports the Te


Diseases in 2

olism for pro

Mary Estes3

ediatrics & Mnd Cellular &ent of Virolo

ucose metanal metabolstric bypassf glucose an

LP-2) is an ome and Cmmatory actiP-2 receptor. GLP2R is

endocrine L m cells (ISC) glycolysis ans a key instrto determin proliferatio

and culturedi-guts were

eated with GC-d-glucose the optimal gycolysis-dep

shifted 13Camine in th

ycolysis inhibnteracting wuclear translohe mini-guts

g of glucose the dual (m

feration in after surger

exas Medica


oliferation i

and Xinfu G

Medicine, Bay& Molecular ogy & Microb

bolism (aeric reprogram

s surgery. Vnd cell prolife

enterotrophCrohn's diseions in the gr (GLP2R), ys expressed

cells. Hyporeprograms

nd activatinructive signane if and hon in human/d in Matrigequantified b

GLP-2 (100tracer or Brdrowth of mo

pendent manC-glucose mhe mini-gutbition. c) Uswith GAPDHocation of ps. Conclusifor biosynth

metabolic andthe crypt sry. (This projal Center D

um:

n intestinal

Guan1

ylor College Physiology,

biology, Bay

robic glycolyming of gluc

Very little is feration in inhic hormonease. GLP-gut. GLP-2-inyet its direct

in crypt seothesis and s metabolic fg PKM2 sigal for coupliow GLP2R / mouse min

el. Intracellulby U-13C-d-g0 nM) ± glydU for 90~12ouse mini-gunner. b) Usimetabolic fluts. This meing proteom

H (a key glypyruvate kinaons: We coesis to suppd mitogenic)stem cells, ject was sup

Digestive Di

l stem

of Yale lor

ysis) is cose is known

testinal e, and -2 has nduced t action

ecretory Aims: fates of gnaling ng ISC directly ni-guts. lar 13C-glucose ycolysis 20 min.

uts; and ng LC-

uxes to etabolic

mics, we ycolytic ase M2 onclude port cell ) signal a key

pported seases

The

Audrey M. Nilotpal RoChristine A By 2020, pcancer-relarefractory metastatic mutagenespancreatic significantldevelopingprotein p12Misexpressin pancreapathogeneexpressionp120 catecytoplasmipancreatic of p120 camodel of acceleratioKCiMist1p12KCiMist1p12pancreatic pancreatic Lineage trQuantificatcells in KMicroarraysignificant results sugpancreatic

Tex 6th Fron

cytoskeleta

Hendley, Yuoy, Hao Ho, A. Iacobuzio-

pancreatic cated deaths to chemoth

burden. sis system w

cancer gey enriched i

g metastatic 20 catenin, sion of p120atic cancer

esis of pancn in human nin to the c staining, wneoplasia,

atenin duringpreinvasive

on of acina0wt/wt pancr0f/f pancreaarea occupinsufficienc

racing reveation of isolatKCiMist1p120f/

y analysis shdifferential

ggest a critcancer.


al regulator p

ue J. Wang, Albert B. Re-Donahue, S

cancer is esin the Unite

erapeutic aA study c

with an oncenes identifiin Kras-driveprogressionwhich is in

0 catenin in ppatients ye

creatic cancepancreatic icytoplasm a

which led usbefore the o

g early Kras-pancreatic

r to ductal reases one ases are sigpied by fibrocy and die aled remarked epithelial/f pancreashowed >126gene expreical role for


nflammator

p120 Catenpreinvasive

Janivette Aeynolds, MatSteven D. Le

stimated to ced States. nd treatmen

combining togenic Krasied genes en neoplasian of pancretegral in staprimary reseet, the mecer are not cintraepitheliaas early ass to hypotheonset of pan-driven panc

cancer, KCmetaplasiamonth po

gnificantly lastroma. Ason average kable epithel cells in the es vs. 15/3 differentia

ession in PIr p120 caten


20

nin supprese pancreatic

Alsina, Ishrat tthias Hebroeach and Jen

climb from tThis deadly

nt regimensthe SleepinsG12D allele iencoding aa with Ctnndatic cancer.abilization ofected pancrechanisms byclear. We al neoplasias PanIN2. size that p1

ncreatic ductcreatic neoplCiMist1. KCiM

a (ADM) anst tamoxifearger than a result, KC8 weeks e

elial cell deextensive s

/7000 CK19ally expresse3K/AKT andnin in regul


Diseases in 2

sses epithec cancer

Ahmed, Haook, Anirban Mnnifer M. Ba

the 4th to thy disease ha, and patien

ng beauty tin mice as aadherens and1 as a locu Ctnnd1 ef cadherin meatic tumorsy which p1comprehens

a (PanIN) an3/5 PanIN320 catenin mtal adenocalasia, we abMist1p120f/f pnd PanIN fen injection.KCiMist1p120CiMist1p120f/f

earlier than elamination stroma revea9+ cells in ed genes! Id Cdc42 sigating epithe


lial cell dela

o Zhang, SaMaitra, Michaailey

he 2nd most as continuednts often extransposon a screen to nd tight junus commonncodes the molecules as correlates w20 catenin

sively examnd identified3 examinedmay play a crcinoma. To

blated p120 cpancreases formation w. At the

0wt/wt pancreaanimals havtheir KCiMist

in KCiMist1paled a strikin

KCiMist1p12PA pathwaygnaling. Taelial cell del

um:

amination in

amuel Savidgael Goggins

common cad to remain xperience a

random in identify cannction protely mutated iadherens ju

at cell membwith worse s

contribute mined p120 cd mislocaliza had predocritical role io examine tcatenin in a display sig

when compasame time ases with 9ve severe ext1p120wt/wt co

p120f/f pancrng 832/700020wt/wt pancry analysis reaken togethlamination i

n

ge, s,

ause of largely heavy

nsertion ndidate eins as in mice unction branes. survival to the

catenin ation of ominant in early the role mouse nificant

ared to point, 92.89% xocrine ontrols. reases. CK19+ reases. evealed her, our n early

Unbiased

Girish S. HStraub, PhLester, B.SOlive, M.Da Section oof MedicineUniversity Center, UnDepartmenand Immun* Correspo

Introductio(EE) has bclinicopathesophagusesophageatissue proteAims: To SNO) in esfrom healthMethods: proximal aand 7 Conand ratio-orobotic picmass speccomponenwestern bloResults: Bwas noted controls rerevealed asubjected twere conupregulateproteins wgalactose-s>1.6 fold inConclusioprotein abudisease phrelated eso

Tex 6th Fron

Proteomic

Hiremath, M..D.b, Christin

S.e, Susan S.a, Alexande

of Gastroentee, Houston, of Texas Me

niversity of Tnt of Pediatrinology, Depaonding autho

on: Esophabeen describological co

s which canal lumen. Altein alterationdetermine r

sophageal tishy children.

Proteins wnd distal esotrols (≤ 1 eo

of-ratio (RoRcking, and actrometry (Mt analysis, aot of tissue sBoth groups

in 67% of ceported anya total of 6to protein idesidered hig

ed and 3 prohere 6 werespecific lectn PE biopsieon: Our unbundance sighenotype anophageal rem


Analysis o

D. M.P.Ha, Jna Nance, Ptafford c, Ko

er Kurosky, Perology, HepTX 77030 U

edical BrancTexas Medicaics, Baylor Cartment of P

or

agus is typibed in assocondition cha eventually though somns remain unrelative globssue obtaine

were extractophageal (Pos/hpf with n

R) exhibiting analyzed by MALDI TOF/Tand unsupervsamples.

were compchildren with y food allerg648 proteinsentification bgh confidenoteins were de upregulatetin involved es and >2.1 fbiased protegnature. Withnd may be amodelling. A


nflammator

f EsophageG

John E WiktoPh.D.c, Melinonrad PazdraPh.D.b,c Carlpatology and

USA b Departch, Galvestonal Branch, G

College of MPediatrics, Ba

cally devoidciation with earacterized result in epe molecularnclear.

bal protein aed from child

ted and seE and DE, r

no histologicp≤0.05 and matrix-assis

TOF). The pvised hierarc

parable for aEE and the

gy. Proteoms, and 91 by MALDI Mnce identificdown-regulad and 8 werin acute allefold in DE bi

eomic analysh western ba major con

Additional stu


21

eal Eosinop

Galectin-3 orowicz, Ph.da Mata, M.

ak, M.D., Pha M Davis, Md Nutrition, Dtment of Bion, TX 77555

Galveston, TXedicine, Houaylor Colleg

d of eosinopeosinophilic by eosinop

pithelial-mesr mechanism

abundance adren with EE

parated by espectively)

c evidence oratios of ab

sted laser dproteins abuchial cluster

age, gendere median eosmic analysisstatistically

MS, and the 6cations. Eigated in PE. Dre down regergic inflammopsies. sis of EE alot confirma

ntributor to eudies to conf


Diseases in 2

philia Revea

.D.b,c, Kizhak

.S.c, Norma .D.b,c, KalpeM.D. e* Department ochemistry a5 USA c The X 77555 USuston, TX 77e of Medicin

phils. Persisesophagitis

phil driven enchymal tr

ms related to

and redox sE compared

2D-gel ele) biopsies obof inflammatibundance andesorption ioundance wasing. Candida

r, and preses/hpf was 38s of mucossignificant

62 exhibitingght uniqueDE containeulated. Exprmatory resp

and normal ation, Gal-3 aeosinophilic firm these fin


als Different

ke V SomanQuintanilla,

esh Thakkar,

of Pediatricsand Molecula

UTMB NHLSA d Section 7030 USA e Sne, Houston,

stent esoph(EoE) - an inflammatio

ransition ando EE have b

state (cysteito esophag

ectrophoresisbtained fromion). Normand RoRs≥1.5onization tims analyzed bate proteins

enting sympt8 (range: 17

sa from pat(p≤0.05) p

g protein sco proteins

ed more differession of g

ponses, was

esophagealappears to esophagea

ndings are u

um:

tial Express

n, Ph.D.b,c, CM.D.d , Mar

, M.D.a, Anth

s, Baylor Coar Biology, BI Proteomiof PathologSection of A, TX 77030 U

hageal eosinallergen-meon limited d narrowingbeen identifi

inyl-S-nitroseal tissue ob

s (2DE) from 6 children w

lized spot vo5 were selecme-of-flight tby t-tests, pwere confirm

toms. Food 7-100). Noneients and crotein spots

ores of 56 orwere signi

erentially abalectin-3 (G

s uniquely el

reveals a be associatel inflammatio

underway.

sion of

Christof rian hony P.

ollege

cs gy, Allergy USA

nophilia ediated,

to the g of the ed, the

ylation; btained

om 2-4 with EE olumes cted for tandem rincipal med by

allergy e of the controls s were r higher ficantly

bundant al-3), a levated

distinct ed with on and

Jian Yang1

1USDA/ARHouston, TStation, TX The prevainfluence oalterations honeysuckdetected inRNAs coulsmall RNAhours afteruptake of were of diemice and gwithout diealtered peconsumersincidence oacids are relationshipopen up ne

Tex 6th Fron

Gut dy

1, Lisa M. Fa

RS Children'sTexas 77030X 77845

ailing sciention the health

in intestinalkle (Loniceran the sera ald also be d

As appear inr the honeysgavage fed etary origin.gavage-fed eetary manipurmeability a

s. We propoof exposureabsorbed a

p between ew vistas for


ysfunction pb

armer1, Abia

s Nutrition R0; 2Vegetable

ific view suhy; howeverl permeabilitra japonica) and urine ofetected with

n circulation suckle was exogenous Cisplatin, aexogenous mulations. Mand gut arcose a mode to dietary sand functionhealth and r gene thera


nflammator

permits the between pla

A. A. Agyek

Research Cee and Fruit I

uggests the r, our data sty may uptak

containing f animals. Ihout gavage after severaremoved froRNAs and

a chemothermiRNAs couicroscopic ihitecture in l where an small RNAs.ning in the nutrition, hepy.


22

transmissioants and con

kum1, Ismail

nter, Baylor mprovemen

consumptiosuggest that ke and circu

diet, gavan the honeyfeeding. In

al days on thom the diet. digital drop

rapy drug, wuld be detectnvestigationthe cisplatarray of die Establishinconsumer

elp establish


Diseases in 2

on of genetnsumers

Elbaz1, Ken

College of Mnt Center, Te

on of plant-consumers

ulate these Rage fed micysuckle fed n the honeyshe diet and RT-PCR d

plet PCR showas used toted in the se

n and FITC-in mice, buets and diseng conditions

will drastich useful die


tic Informat

ndal Hirschi1

Medicine, 11exas A&M U

-based dietawith diet or

RNAs. AftercroRNAs (mpopulation,

suckle fed awere no lon

demonstrateowed that th

o induce gutera of the cisDextran ass

ut not in theease states s whereby dally alter o

etary practice

um:

tion

, 2

100 Bates Sniversity, Co

ary RNAs hr substance-r several daymiRNAs) co

plant basedanimals, the nger detecta

ed dose dephe amplifiedt/kidney damsplatin-treatesays demone honeysucmay influen

diet-derived ur concept es, and pot

treet, ollege

has no -related ys on a

ould be d small dietary

able 48 pendent d RNAs mage in ed mice nstrated kle fed nce the nucleic of the

tentially

Norw

HutchinsonFrederick HGraham, D 1Interdepar2Departme3Alkek Cen4Departme5Human G*Currently a The gut mreplication intestinal mchallenge participatedsamples cmicrobiota not associanot associadays post-Among themore stabshedding).Subdoligrashedders. compositiodemonstrapotential forelationshipreplication

Tex 6th Fron

alk virus sh

n, Diane S1,2

H2; Opekun, David Y2,4; At

rtmental Proent of Molecunter for Metaent of Medicienome Sequat University

microbiome cand syste

microbiota, study. The d in an expeollected at drelated to N

ated with suated with thchallenge, th

e 20 infectedble when co Furtherm

anulum variaThe results

on. Howeveated that loor butyrate pp between tin the huma


hedding dur

2,3; Ajami, NaAntone R2,4

tmar, Robert

ogram in Traular Virologyagenomics ane uencing Ceny of Michigan

contributes tmic pathogand the hustudy popu

erimental chadays -7, 2, Norwalk viruusceptibility te presence he microbiomd individualsompared to

more, metaabile, a buty

indicate thaer, microbioong shedderproduction thhe microbio

an host.


nflammator

ration is ass

adim J2,3; Wo4; Metcalf, Gt L1,2,4; Estes

anslational By and Microband Microbio

nter, at Baylon Medical Sc

to the deveenesis. We

uman host ulation consallenge with4, 8, 21, ans infection. to NV infectof gastroen

me composi, the microb

o pre-challenagenomic syrate producat Norwalk vme stabilityrs maintainhroughout Nme and inte


23

sociated wi

ong, Matthewinger A5; Mus, Mary K1,2,4

iology and Mbiology me Researc

or College ochool

elopment of e assessed in fecal sa

sisted of 46 Norwalk vir

nd 56 were The pre-chation, and micnteritis or sption of infect

biome of longnge than thsequencing cer, and butvirus infectioy is associ a stable

Norwalk virusestinal health


Diseases in 2

ith stability

w C2,3, Finkbuzny, Donna4; Petrosino,

Molecular Me

ch

of Medicine

gut immunithe interac

amples colle6 geneticallyrus, the protanalyzed to

allenge fecacrobiome coecific symptted and uning shedders (hat of shor

revealed tyrate metab

on is not assiated with microbiomes infection. h may impro


of the feca

beiner, Staca M5; Gibbs, , Joseph F1,2

edicine

ity and enhaction betwe

ected from y susceptibotypical noroo assess chl microbiom

omposition ptoms. At prenfected indiv(≥ 18 days vrt shedders

increasedbolism pathwsociated withviral shedd

e characteriFurther cha

ove understa

um:

al microbiom

cy R2*; Neill, Richard A5;

2,3

ances entereen noroviruthe Norwalle individuaovirus strain

hanges in the compositiopost-challenge-challenge viduals was viral sheddin

(≤ 14 dayd abundanway genes h fecal microding duratiozed by incracterizationanding of no

me

ric viral us, the k virus

als who n. Fecal he fecal on was ge was and 56 similar.

ng) was ys viral ce of in long obiome

on. We creased n of the orovirus

BS1

HS

Store-o

Budi Utama1

Sue E. CrawMolecular V

Houston, TXSummer Res

Rotavirus (Rlicensed vavivo, and nmechanismof RV infectCa2+ stores RV replicati(NSP4) is amechanismintegrated tforms a Ca(SOCE) andsubsequentdiarrhea. Wbiosensors.expressing luminal Carecombinanfailed to ac(HEK293FTwe found tchannel, mocell line to and blockinmediated Cinflux inhibiUnexpectedreplication express thereplication, NSP4 releaincluding SCaCC chlonorovirusesgastroenterstudied as p

This work wwhich suppo

Tex 6th Fron

operated anmediat

, Nina K. Rawford1, KhalilVirology & MX. 3Biochemissearch Intern

RV) is the leaccines, caunewly devels of RV-indtion is elevaand Ca2+ e

ion and thoua viroporin (vs of how NSto chloride sa2+ channel d voltage-actly activates

We have ge To evaluYFP-tagged2+ that activ

nt NSP4 expctivate YFPT) and humahat RV induost potently measure Cl-

ng Ca2+ entCa2+ entry isitors all redudly, L-type vand we dis

e Cav1.3 VAsuggesting

ases ER Ca2

OCE and Voride secretis) disrupt hitis. If so, potential ant

was supporteorts the Tex


d voltage-ated viropor

amachandra Ettayebi1, Microbiology astry & Cell Bnship Progra

ading causeses >450,00oped humauced changted cytoplasntry throughught to contviral pore-foSP4 viroporisecretion an

to release ctivated (VA

Ca2+-activaenerated a uate effects d stromal intvates SOCEression activ-STIM1 and

an intestinal uced Ca2+ eby the drug

- secretion, try through critical for uced RV yievoltage-activscovered thaACC. Specifi

Cav1.3 is i2+ to activateVACC channion and suost Ca2+ sidrugs targeiviral drugs t

ed in part bas Medical C


nflammator

activated carin activity t

an1,3, Alicia CMary K. Esteand 2Molecu

Biology, Riceam, Rock Isl

e of viral chil00 deaths wn intestinal es in Ca2+ s

smic Ca2+ ([Ch plasma meribute to sec

orming proten activity disd diarrhea rluminal ER

ACC) Ca2+ cated chloride

series of sof NSP4 o

teraction moE upon ERvated YFP-Sd did not in(Caco2BBe

entry was in 2-APB. Preindicate theOrai1 with Cl- secretioeld, underlin

vated Ca2+ cat human eic VACC bloimportant fo

e STIM1, trignels. This gpports RV gnaling, ma

eting cellularto reduce ga

y NIH grantCenter Dige


24

alcium chanhrough rele

C. Strtak1,4, Des1, and Joseular Physioloe University, land, IL.

dhood gastrworldwide. O

enteroid msignaling thaCa2+]c) causembrane (PMcretory diarr

ein) and this srupts host Cremained un

R Ca2+ and hannels in t

e channels (stable cell on SOCE,

olecule 1 (YFR Ca2+ storeSTIM1 and encrease [Cae) cell lines snhibited by eliminary rese Anoctamin

2-APB inhn, which is ning the impchannel (VAnterocyte cockers inhibor RV-induceggering Ca2+

global disrupreplication.

aking theser Ca2+ chanastrointestina

s DK093657stive Diseas


Diseases in 2

nnels are acease of ER

Doug Peterseph M. Hyse

ogy & BiophyHouston, TX

roenteritis anOur studies model systemat contributesed by releasM) Ca2+ charhea. We sh function eleCa2+ homeoncharacterizER Ca2+ dethe PM. Ca(CaCCs) to lines that ewe generat

FP-STIM1), e release. elevated [Caa2+]c. Using stably expremultiple blo

sults using a1 (Ano1) C

hibited CaCClikely respoportance of

ACC) blockeell lines an

bited both Ned Ca2+ upt

+ entry througption of Ca2

It is posse pathways nels, such al virus-indu

7, U18-TR00ses Center


ctivated by rcalcium sto

s1,4, Alexandrer1 ysics, BaylorX. 4Augusta

nd, despite iuse a comb

ms to undee to diarrhease of endopnnels, all of

howed RV nevates [Ca2+

ostasis and hzed. We hypepletion acta2+ entry thrinduce Cl- s

express fluoted a biosean ER transWe found

a2+]c, but a N both huma

essing a GFPockers of tha halide-quenCaCC is stroC activation

onsible for df this procesers also signd human inSP4-inducetake. Our sgh host Ca2

2+ homeostaible other ea general

as Orai1 anuced diarrhea

00552, AI08

um:

rotavirus Nores

ra Chang-G

r College of na College T

implementatbination of irstand the

al disease. Alasmic reticuwhich is esonstructural+]c, but the how these spothesized tivates storerough these secretion thorescent Caensor cell lismembrane that RV inf

NSP4 viropoan embryonP-based Cahe SOCE Onched YFP-

ongly activatn, suggestindiarrhea. SOss for RV renificantly redntestinal ented Ca2+ entrstudies show2+ channels iasis directly enteric virusmechanism

nd Cav1.3, sal disease.

80656, and

SP4-

raham1,

Medicine, TMC

tion of two in vitro, in molecular

A hallmark ulum (ER) sential for protein 4 molecular ignals are hat NSP4

e-operated channels

at causes a2+ or Cl- ine stably sensor of fection or rin mutant

nic kidney a2+ sensor, Orai1 Ca2+ -biosensor ted by RV ng SOCE-OCE Ca2+ eplication. duced RV teroids all ry and RV w that RV in the PM,

activates ses (e.g.,

m for viral should be

DK56338,

Special co

Faith IhekwClaire Bocc

1Section ofTexas ChilHospital, H4Departmeof PediatricChildren’s BACKGROrecurrent (must be taunderlying evaluate tincorporatiMETHODSfrom screeprotocol, fdisease (1significant day prior aThe fecal mRESULTS2 months fmonths aftHe was coconvergenhowever, radults. BasymptomaOut of the difficile direThe UC psubsequenOne patien2nd enemaCONCLUScomplicatinthe coursedonor baccarriage mwhen cons

Tex 6th Fron

onsideration

weazu1, Emichini5, Ruth

f Pediatric Gdren’s Hosp

Houston, TX,ent of Patholoc Infectious Hospital, Ho

OUND: Fecantibiotic re

aken with peclinical con

the microbiaon of these

S: Nine rCDened, self-defollowed by 1 ulcerative neurologic

and 8 weeksmicrobiomes: All 4 patienfollowing a ster FMT durionsidered ance of the rremained asacteroidetesatic carriage5 patients wected antibiopatient requnt clinical cont was diagna FMT. SIONS: FMTng clinical coe of rCDI incterial speci

may predisposidering FMT


ns for fecal

ly Hollister2,4

Ann Luna2,4

Gastroenteropital, Housto, USA; 3USDogy& ImmunDisease, Deouston, TX,

cal microbiofractory) Cloediatric rCDnditions wheal mechanispediatric coI patients (1esignated orenema FMcolitis [UC

impairment s after the firs were studients without usingle FMT.ng an uppern asymptomrecipient mis distant fros specificae of C. difficilwith complicaotic therapieuired FMT 3ourse. The Cnosed with

T is highly onditions. Cldicates a faes and rec

ose to CDI. T for rCDI in


nflammator

microbiotadiffic

4, Dorottya N4, James Ver

logy, Departn, TX, USA;

DA/ARS Chilnology, Baylepartment ofUSA

ota transplaostridium difI, given a h

en comparedsm of actionsiderations.5-16 year or universal d

MT, if clinica], 1 Crohn as underlyinrst FMT. Seed by 454 pyunderlying d One of ther respiratory

matic carrier.crobiomes

om the donolly increasle did not sigating clinical es prior to F3 times to

CD patient’s poorly mana

effective forlinical improavorable outconstitution A special appediatric pa


25

a transplantcile infectio

Nagy-Szakarsalovic2,4, a

tment of Ped 2Departmenldren's Nutritor College of Pediatrics,

ntation (FMfficile infectiohigher asympd to adults. on of FMT s. old) receiveddonors throu

ally indicateddisease [C

ng conditionlect patientsyrosequenciisease had r

ese patients infection, b. Metagenomto the donoor microbiomed in abugnificantly mconditions,

MT. These clear CDI, diarrhea didaged consti

r the treatmvement duritcome followof recipientpproach inco

atients with u


Diseases in 2

tation in pen

l1,3, Abria Haand Richard

diatrics, Baynt of Patholotion Researc

of Medicine, Baylor Colle

MT) is the on (rCDI). Sptomatic caWe performin a cohor

d filtered, frough colonosd. Two pati

CD]), 1 had ns. All patiens gave additng of the baresolution ofwas found

ut was withomic analyseor’s microbime as indeundance fo

modify microbonly 2 had opatients resbut still re

d not responpation and

ment of pediing C. difficilwing FMT. Ft microbiomorporating t

underlying di


diatric recu

aynes2,4, MilKellermayer

ylor College ogy, Texas Cch Center, HHouston, TX

ege of Medic

most effecSpecial consrriage rate a

med metagert of rCDI

ozen-thawedscopy underients had in

heart transnts providedtional samplacterial 16S f their symptto be positi

out gastrointes indicated iome. Recip

ependent heollowing FMbiome compobvious clinsponded weeceived colend to either C. difficile c

iatric rCDI ile directed aFMT results

mes. Asympthese findingisorders.

um:

urrent Clost

ena Pitashnr1,3

of Medicine,Children’s Houston, TXX, USA; 5Secine, Texas

ctive treatmesiderations foand more fr

enomic analypatients, w

d fecal prepr an IRB apnflammatorysplant, and d a stool saes to be anrRNA gene. toms for move for C. diftestinal comthat FMT in

pient microbealthy childreMT. Intere

position. ical benefit f

ell to a singleectomy duriantibiotics o

carriage dur

in patients wantibiotic thes in engraftmtomatic C. gs should be

tridium

ny2,4,

,

, USA; ection

ent for or FMT requent yses to

with the

paration pproved y bowel

2 had ample 1 alyzed. re than fficile 4 plaints. nduced biomes, en and

estingly,

from C. e FMT. ing his

or FMT. ing her

without erapy in ment of difficile

e taken

Li Jiao1,3, NMatthew WKanwal1,3, 1Departme3Section of Backgrouintestine, ain healthy i Methods: colonoscopand July 20cecum, ascsamples wfrom sampplatform. T(OTU) clas Results: WcomparablProteobactincrease asamples shsubject hadEscherichiathe compolevel. Varialevel. The a more equdiversity anindividual rrectum from Conclusioamong eacimplicationenvironme

Tex 6th Fron

Character

Nadim J. AjaWong2, Bhup

Maria Velez

ent of Medicif Gastroente

nd: Our undas well as onindividuals is

We enrolledpy suite at th014. We obtcending, tran

were also colples and the The sequencssification an

We obtained e amounts oteria accounbundance ofhowed an ind unique mica_Shigella, Asition of the

ations in comShannon divual distributinalysis (weigrather than bm other segm

ons: The intrch individual of mucosal ntal determi


ristics of m

ami2, David Ginderjit Anan

z1,3, Donna L

ne and 2Molerology, Mich

derstanding on the diversits limited.

d eight men (he Michael Etained a totansverse, deslected from 16S V4 regi

cing data wend calculatio

~3,450 seqof OTUs idennted for > 95f Proteobactcrease in Ficrobiota signAkkermansimucosal mi

mpositions wversity indexon in the abghted UniFraby sample sement.

ra-individual l. Mucosal mand fecal mnants of lon


nflammator

ucosal and

Graham1,3, Ynd1,3, RhondL. White1,3, H

ecular Virolohael E. DeBa

on longitudinty at lower ta

(age: 51-69 E. DeBakey al of 38 snapscending, sigthree men bon was ampre analyzed n of diversity

uences for entified for ea% of both mteria comparrmicutes andnature. Variaa, and Faeccrobiota alo

were seen fox scores werundances ofac PCoA) suegment. For

microbiota dmicrobiota wamicrobiota in

gitudinal var


26

fecal micro

Yasser Shaibda Cole1,3, CHashem El-S

ogy and Micakey VA Me

nal spatial daxonomic lev

years old, foVA Medical

p frozen normgmoid, and

before bowelplified and se

using QIIMEy indices.

each sampleach subject.

mucosal and red to colonid Bacteroideations in comcalilbacteriumng the larger Akkermansre higher for f the OTUs f

uggested thar the same in

diversity wasas under-precolon tumorriation of mic


Diseases in 2

obiota in he

b1,3, Jocelyn lark Hair1,3,

Serag1,3, Jos

robiology, Bedical Cente

iversity of mvel between

our non-HispCenter in H

mal colonic mrectum segml cleaning. Mequenced usE v1.8 for op

e. Feces andBacteroidetefecal sampleic mucosa, Ietes comparmposition wem at the Gene intestine resia and Lachcolonic muc

found in mucat the microbndividual, the

s greater thaesented in thrigenesis macrobial comm


ealthy indiv

Uriostegui1,

Jason Hou1,

eph F. Petro

Baylor Collegr

mucosal micr mucosal an

panic white) ouston betwmucosa surfment of the iMicrobial DNsing the Illumperational ta

d colonic mues, Firmicutees. NonetheIn contrast, cred to fecal sere seen for nus level. Foemained stabhnospiraceacosa than focosal samplbiome was ce separation

an the inter-he fecal samay be differemunity shou

um:

iduals

,3, Liang Che,3, Fasiha osino2

ge of Medicin

robiota in thend fecal micr

from the ween July 20face biopsiesintestine. ThA was extramina MiSeq axonomy uni

ucosa had es, and

eless, feces colonic mucosamples. EaLachnospira

or each subjeble at the ph

ae at the genor feces sugge. The beta-

clustered by n was seen f

segment divmples. The ent. Host andld be investi

en1,3,

ne

e large robiota

013 s from

he fecal acted

t

had osal

ach aceae, ect,

hylum nera gesting -each

for

versity

d igated.

Effects o Coreen Joand James 1Departme2Departme

Probiotics as inflammmicroorgancomponendecarboxyinflammatothe primaryproject soustudies shoinflammatogroups witshowed deby modulat

Tex 6th Fron

of L. reuteri

hnson1,2, Bhs Versalovic1

ent of Patholoent of Patholo

may affect tmatory bownism, Lactot, L-histidinelase. The p

ory cytokine y contact of ught to identowed that L.ory cytokine thout histamecreased expting pro-infla


derived his

hanu Priya G1,2

ogy and Immogy, Texas C

the disease wel diseasebacillus reu

e, to the bioproduced hisTNF in humthe L. reuteify how hista. reuteri deriIL-8 by HT

mine. In addpression of ammatory cy


nflammator

stamine on

Ganesh1,2, M

munology, BChildren’s H

course of pe via moduteri ATCC logically actstamine from

man myeloid eri derived hiamine affectived histami

T-29 cells stition, HT-29IL-8. Overaytokines


27

IL-8 expres

onica Lugo1

aylor CollegHospital, Hou

atients with ulation of PTA 6475,

tive immunom L. reutercells thereb

istamine is ts the expresne significantimulated wi9 cells treateall, L.reuteri d


Diseases in 2

ssion using

,2, Vanessa

ge of Medicinuston, Texas

chronic immthe host

, has been oregulatory sri has been by modulatinthe intestinassion of cytontly suppresith IL-1β, coed with comderived hista


in vitro cel

Jackson1,2

ne, s, USA

mune-mediaimmune sy shown to

signal histamshown to

ng host immal epithelial cokines from esses the expompared to mmercially aamine show

um:

l culture mo

ated disorderystem. One

convert a mine via a hsuppress thunity. Howe

cell (IEC) layepithelial cepression of tthat of the

available hisws beneficial

odels

rs such e such dietary istidine

he pro-ever, as yer, our lls. Our he pro-control

stamine effects

Systemic

Sunkuk Kw 1 Center foThe Univer 2 The UniveThe Univer Backgrouconditions important rmanifestatlymphatic farchitectur Methods: nitric oxidedisease acmethyl esteFL-C16. Lusing dynaindocyanin Results: Dthe skin of the mesenlymphatic vmice expossignificantlDSS treatmreduced asDSS-colitislymphatic pperipheral profile and Conclusioinvasively inflammatio

Tex 6th Fron

cally-altered

won,1 Germa

r Molecular rsity of Texa

ersity of Texrsity of Texa

nd: Altered including inf

role in the paions. Howevfunction. Thre are system

In the acutee synthase (ictivity. Mice er (L-NAME

Lymphatic coamic near-infne green (ICG

Dynamic NIRmice exposteric lymphavessels in thsed to DSS y higher freq

ment, the cos compared s mice treatepump activitylymph node dendritic ce

ons: Our stumonitor lympon and prov


d lymphatic

aine Agollah

Imaging, Thas Health Sc

xas Graduateas MD Ander

lymphatic fuflammation. athogenesis ver, it is unk

he aim of ourmically altere

DSS colitis NOS-/-) werwere also tr). Mesenter

ontractile funfrared fluoreG) to the hin

RF imaging ded to DSS.

atic vessels, he skin of mifor 4 days squency thanntractile freqto their resp

ed with L-NAy. Additionas of mice wi

ell migration.

dy demonstrphatic functiide informat


nflammator

c function in

,2 Grace Wu

e Brown Focience Cente

e School of rson Cancer

unction and s Recent datof inflamma

known if, andr study was ed in dextran

model, Balbre fed with Dreated with bric lymphaticnction and veescence (NIRnd paw in mi

data demonsMice with abut not in dece with DSShowed simil wild-type m

quency in bopective baseAME showedlly, histologyth DSS-indu.

rates showson and vession about re


28

n mice with

colitis

u,1 and Eva M

undation Inser, Houston,

Biomedical Sr Center, Ho

structure areta suggests tatory bowel dd how local ito investigatn sulfate sod

b/c and C57BDSS in the drboth DSS anc vessels weessel remodRF) imaging ce prior to a

strated systecute colitis sermal lymph

S-induced coar lymphatic

mice with the oth iNOS-/- alines and did

d partial but y and fluoresuced colitis r

s the feasibilisel remodelinesponse to th


Diseases in 2

dextran-su

M. Sevick-M

stitute of MoTX 77030,

Sciences at ouston, Texa

e implicated that the lymdisease (IBDnflammationte whether lydium (DSS)-

BL/6 mice arinking wate

nd a NOS inhere visualizedeling were lofollowing in

and 4 and 7

emically impshowed impahatics. Howeolitis. The lyc contraction same treatm

and wild-typed not statistinot completscence activreveal altere

ity of functiong in systemherapy.


ulfate sodium

Muraca1

lecular Med

Houston, as 77030,

in a numberphatic systeD) and extran in the gut aymphatic fun-induced acu

and mice lacker and monitohibitor, NG-nd after oral gongitudinallytradermal (i.days after D

aired lymphaaired lymphaever, we obs

ymphatic vesn frequency ment. Howeve mice was cally differ fre improvem

vated cell soed architectu

onal NIRF immic lymphatic

um:

m-induced

icine

r of pathologem may playintestinal affects systenction and ute colitis.

king inducibored to asse

nitro-l-arginingavage of Boy characteriz.d.) injection

DSS treatme

atic contractatic drainageserved dilatessels in iNOSas baseline,ver, at 7 daysignificantly rom each otent of systerting analysire, leukocyte

maging to noc response t

acute

gical an

emic

le ess ne odipy-zed n of nt.

tility in e in ed S-/- , but ys of

ther. mic is of e

n-to

C

Eric E. LloyRobert Bry 1Dept. of A3Texas ChiHouston, T Individualsrepeatedlycerebrovascerebral smbrain. CSVgrey mattealterations spontaneochronicallyassigned tapneas, cinstrumentcontinued through sethe Firmicsignificantlrespectivelincreased of microglmorphomepretreatingdrinking wrats, OSA damage tomicroglia (hypertensiostudy furthconsequen

Tex 6th Fron

erebral Sm

yd, PhD1, Dayan Jr, PhD1

Anesthesiologildren’s MicrTX, USA.

s suffering f collapses scular diseamall vessel VD produceser. In the pre

to the guusly hypert

y instrumenteto an OSA correspondined with a traeach day fo

equencing ofcutes:Bacteriy increased ly. Blood bra(n=6, p<0.05ia, the resi

etric analysig the SHRSPwater), which

induced no o the blood (n=4-9, p=0on, blood-bher suggesnces of OSA


all Vessel D

avid J. Durga.

gy, 2Dept. ofobiome Cen

from obstrucduring sle

ses or accedisease (CSs cognitive sent study w

ut microbiomtensive stroed with a tragroup, whe

ng to severacheal balloor 8 hr durinf the bacteriiodetes ratio(n=7-10, p<

ain barrier p5) in small vident immuns) in the OP OSA grouh dramatical

significant cbrain barri

0.001). Ourrain barrier

sts that bacA.


nflammator

Disease, Ob

an, PhD1, Em

f Pathology anter, Departm

ctive sleep eep to prolerating the

SVD), involvimpairment,

we tested theme (i.e., dyoke prone racheal ballooere the ballore OSA in

oon but wereng the sleepal 16s rRNAo (from 0.7

<0.05) in SHpermeability,vessels of thne cells in OSA group p with antibly decreasechange in ther (n=4-9, r studies linintegrity, an

cteriotherap


29

bstructive S

mily B. Hollis

and Immunoment of Path

apnea (OSoduce apneprogressiones patholog, resulting fre hypothesisysbiosis) resrats (SHRSon that couldoon was inf

humans, oe not subjecp cycle for 2A gene in fec76 to 0.48, RSP with O, as assesse

he OSA groubrain was compared

biotics (ampied Firmicutehe systolic bp=0.015), ank gut dysbnd activatioy could po


Diseases in 2

Sleep Apnea

ster, PhD2,3,

ology, Baylorhology, Texas

SA), a condea, are atn. One of theical alteratiorom damags that CSVDsulting from

SP), an anid be remotelflated 60 timor to a shcted to apne2 weeks. Ancal samplesp=0.046).

SA by 20 ± ed by IgG eups compare

significantlyto sham ccillin [1 gm/

es:Bacteriodeblood pressu

and attenuatbiosis, occun of residenossibly blun


a, and Gut D

Julia L. Cop

r College of s Children’s

ition where t risk for ese cerebroons to the sme to cerebr

D is acceleram OSA. 15imal model y inflated. R

mes/hr for 1am control as. In the Onalysis of ths, revealed aSystolic blo4 mm Hg ab

extravasationed to sham cy greater (

controls (n=/L] and neometes ratio inure (n=4-9, ted or aboli

urring as a nt immunitynt some of

um:

Dysbiosis

pe, PhD2,3, a

Medicine, Hospital,

the upper either deve

ovascular dismall vesselsal white andted by patho to 20 we

for CSVDRats were ra10 sec to p

group thaOSA group, ahe gut microa significant ood pressurbove the shan, was signicontrols. Acas determin6, p<0.05). mycin [0.5 gn another stp=0.478), reished activaresult of O

y in the braf the patho

and

airway eloping seases, s of the d deep ological eek old , were ndomly

produce t were apneas

obiome, shift in

re was am rats ficantly tivation ned by

When gm/L] in train of educed ation of OSA, to

in. Our ological

SPDEF in

Lo, Yuan-H 1. IntegrativMedicine 2

Center 3. D Backgrouthat resultconditions,and differefrequently β-catenin tmolecular between Ntargets andis regulateSPDEF plintestine. Wnegatively SPDEF me Material atranscriptiooverexpresimmunoprestaining. Win vivo by u Results: Wcatenin tarexpressioncatenin-driinteracts wphysiologicInterestingbind to β-cSPDEF binchromatin through probserved freveal metogether, thpathways, tumorigene

Tex 6th Fron

nhibits colo

Hung1,3; Noa

ve Molecular. Division of

Department o

nd: Colorects in the o, Wingless/Ientiation of dysregulatetranscriptiontargeted th

Notch and Wd strategies.ed by ATOHays an impWe have aregulates β

ediated repre

and Methodonal activityssed in humecipitation

We directly ausing inducib

We found thargets, such n, which is ven intestina

with β-catencal conditionly, our resul

catenin or to nds to β-cainteraction.

rotein-proteinfor β-cateninchanistic inhese resultscoordinatel

esis, but also


rectal cancthr

ah, Taeko2; S

r and BiomeGastroenter

of Medicine a

ctal carcinogoncogenic trnt (Wnt) anintestinal e

d. Although al activity is

herapies havWnt/β-catenin

We have shH1, a key gaportant role also previouβ-catenin traession of β-c

s: To invest, tagged w

man CRC ce(co-IP), chnalyzed the ble mouse m

at cellular pras Cyclin Dconsistent wal tumorigen

nin in both ns. The bindlts indicatedinhibit β-cattenin target We propos

n interactionn in this studsights into

s suggest thay maintainino intestinal s


nflammator

er cell growrough prote

Shroyer, Noa

edical Sciencrology, Hepaand Dan L. D

genesis is dransformationd Notch sigepithelium. H

constitutive believed to

ve limited en pathways hown that Satekeeper fo

in cell cycusly reportedanscriptionalcatenin trans

tigate the mwildtype SPDell lines follo

hromatin imeffects of S

model (Lgr5C

roliferation, D1 and c-Mywith our prenesis and shhuman CRding region that the DNtenin transcrsites on ch

se that SPDn, independy. Ongoing eSPDEF fun

at SPDEF mng intestinastem cell bio


30

wth by reguein-protein I

ah1,3

ce (IMBS) Gatology, and Duncan Can

riven by a son of normagnaling pathHowever, inactivation odrive most

efficacy. Thin CRCs mAM Pointed

or Notch-drivcle exit andd that SPDl activity. Hescriptional a

mechanism oDEF or trunowed by β-

mmunoprecipPDEF expre

CreERT2; β-cate

β-catenin trayc, is inhibiteevious studihrinks estab

RC cells in for SPDEF

NA-binding driptional actihromatin, reDEF could ent of its Dexperiments

nction in CRmay be a pivo

l homeostasology.


Diseases in 2

lating β-catInteraction

raduate ProNutrition, C

ncer Center,

series of geal colonic hways coordn intestinal of canonical human colo

herefore, idemay allow de

Domain Etsven differen regulates

DEF is a coere we test

activity in hum

of SPDEF-mncated SPD-catenin tranpitation (Chession in β-ceninexon3; Ro

anscriptionaed in humanes in vivo.

blished tumovitro and m

F and β-catedomain of Sivity. Finally,

esulting in thmediate oth

DNA bindings using ChIPRC and norotal link betwsis and imp


tenin transc

ogram, Bayloincinnati Ch Baylor Colle

enetic and emucosa. Udinately regcancers, thWnt signalinrectal cance

entifying traevelopment os transcriptiotiation of intterminal difolonic tumot the molecuman colon c

mediated inhDEF mutantsnscriptional hIP) and icatenin-driveosa26rtta-ires-E

al activity, ann CRC cell Moreover,

ors in vivo. Imouse intesenin interac

SPDEF is un, our ChIP dhe disruptionher transcripg capacity, sP-seq and Rrmal intestinween Notch pacting not

um:

criptional ac

or College ofhildren’s Hosege of Medi

epigenetic chnder physio

gulate homeese pathwang resulting ers (CRCs), nscriptional of new theraon Factor (Stestinal epitfferentiation or suppressular mechancancer cells.

ibition of β-cs were tranactivity assimmunofluoren intestinal EGFP; TRE-Sp

nd expressiolines after SSPDEF inhn addition, S

stinal cryptsction was mnnecessary fdata suggestn of β-catenption prograsimilar to wNA-seq assanal biology. and Wnt/β-conly on co

ctivity

f spital cine

hanges ological

eostasis ays are

in high current nodes

apeutic SPDEF) helium. in the

or that nism of

catenin nsiently ay, co-rescent tumors

pdef).

on of β-SPDEF ibits β-SPDEF under

mapped. for it to ted that nin and amming

what we ays will Taken

catenin lorectal

Pankajini M 1University2Baylor Co

Fatty liver National H(3 to 23 peto steatohedemonstramorbidity airinotecan based neotreatment associatedirinotecan t In hepatic including involved wliver toxicitof several involves (i)is further glucuronostwo inactivExcess acirinotecan homeostasbias causecomplex di To develop& 50 mg/k10, liver waSignificant Interestingtranscriptiotranscriptiomost likelydirect accudirecting pfatty acid possible pathe powerfDMEs in pa

Tex 6th Fron

An

Mallick1, Mic

y of Houstonollege of Med

disease (Fealth and Nu

er cent). FLDepatitis whe

ated that cheand mortaliwhich is wi

oadjuvant chof CLM by

d FLD and mtherapy is st

steatosis, increasing ith drugs thaty has been drug metab

) Bioactivatiodetoxified

syltransferesve metabolitccumulation

causes FLDsis. Therefored by pre-exisease.

p an irinotecg of irinotecas excised a

steatosis (ly, we found

on factor inon factor invy increased fumulation ofpossible acchomeostasiathogenic mful early stagathogenic m


nimal Mode

hael M Ittma

, Departmendicine, Patho

LD) is one utritional Exa

D manifests aen accompaemotherapyty in these dely used fohemotherap

hepatic resmorbidity/motill not known

fat accumuhepatic FFAat induce FLrelated to e

bolizing enzon by carbo to inacti

ses (UGTs);tes i.e. NPCof the SN-3

D by alteringre, our aim xisting inflam

can-induced can via intra and fixed in (Average std that irinotenvolved in volved in fafatty acid upf triglycerideumulation os. Thus, ou

mechanisms ges of disea

mechanisms


nflammator

el of Irinotec

ann2, and Ro

nt of Pharmaology and Im

of the leadiamination Sas simple st

anied with intreatment patients. O

or the treatmy effectivelysection. Howortality after n and need t

ulation occuA uptake, s

LD seems to nhanced geymes (DME

oxylesterasesive SN-38 (ii) Oxidatio

C and APC.38 causes fag the gene eis to develo

mmation to d

FLD animalperitoneal (10% formaleatosis sco

ecan significafatty acid tty acid me

ptake and/or es. Importanof toxic SN38ur novel in involved in i

ase models tof complex d


31

can-induced

omi Ghose1

aceutical Scimmunology,

ing causes urvey reportteatosis (fat nflammation is associate

Of particularment of coloy down-sizewever majohepatic surto be explor

rs by modisynthase abe diverse a

eneration of Es). Irinotecas (CEs) to f

glucuronidon by cytoc NPC is co

atal diarrheaexpression oop irinotecadetermine th

l model, we (i.p) route foin for fat acc

ore: 2+) wasantly down-rsynthesis, wtabolism. Thdecreased

ntly, the exp8 in the livevivo model irinotecan inthat may prodiseases.


Diseases in 2

d Fatty Live

iences, HouHouston, TX

of chronic lts, in USA oaccumulatio or fibrosis.

ed with FLDr importancorectal liver

es liver metor problem wrgery. The mred.

ifying free fnd reducingand unique. toxic metaban is a prodform more ade (SN-38Gchrome P45onverted to a in cancer of enzymesn-induced Fhe pathogen

treated aduor 9 consecucumulation as observed regulated gewhereas upherefore, it’sfatty acid ou

pression of er that migh

provides vanduced fatty ovide import


er Disease

ston, TX – 7X-77030

liver diseaseover 30 millioon in liver), w. Recent cli

D, which ince is the ch

r metastasisastases andwith irinotec

mechanism o

fatty acid (g oxidationIn certain caolites due todrug and itsactive metabG) by uri0 (CYP) 3ASN-38 by tpatients. W

s involved inFLD animal nesis and ro

ult male C57utive days, oassessment

at both doene expressp-regulated s reasonablutput mechaCyp3a11 wat contribute aluable infoliver. Our sttant new ins

um:

77030

e in the USon adults havwhich can prnical studie

creases the hemotherapys (CLM). Irind thereby ecan treatmeof FLD indu

FFA) home. The mecases, highero increased s biotransforbolite, SN-38dine dipho

A enzymes tthe CEs ene hypothesi

n regulation model witho

ole of DMEs

7BL6J mice wonce daily. Oby H & E st

oses of irinoion of enzymthe enzym

le to considanisms leadsas down-regto the chan

ormation abotudy is indicasights in the

S. Third ve FLD rogress s have risk of

y drug, notecan enables nt was

uced by

eostasis hanism r risk of activity rmation 8 which osphate to form zymes. ze that of lipid out the

s in this

with 25 On day taining. otecan. me and

me and der that s to the gulated nges in out the ative of role of

Dysregu

Maynard, JDolores6; F

1DepartmeLiver CenteCenter, BaBasic Scie6DepartmeBaylor Col Backgroustudies suhepatocytetissues. HoHypothesihepatocellu Methods: uninvoled Hep3B, SNwere validaof purinergand BrdU terminal Ki Results: Mcompared expressionreceptor exsufficient tincorporatiattenuatedP2X3 promdownregulaHCC patiereceptor isgenes of h Conclusiorole for dyphenotype

Tex 6th Fron

ulation of p

Janielle P1,2,

Finegold, Mil

ent of Pediater, 2 Program

aylor Collegence Researc

enf of Pathololege of Med

nd: Hepatouggest that e proliferatioowever, the is: Dysreguular carcinog

P2 purinergareas, n=4

NU387, PLCated by micrgic signaling

incorporationase inhibito

Multiple P2 to uninvolv

n was assoxpression wto induce con and incr nucleotide-moted prolifation of cycl

ents. Mst1/2soforms as ippo signalin

ons: Our anysregulation and identifie


urinergic spatie

3; Johnson, lton J2,3,6; Go

rics, Divisionm in Translae of Medicinech, 5Departmogy and Immicine, Houst

cellular carcextracellula

on in vitro apathophysio

ulation of pugenesis.

gic receptor 2), Mst1/2-/-

C/PRF/5) weroarray (mRon HCC ce

on of HCC or) or AF-35

purinergic ved areas iciated with

was observedcell cycle preased cycli-induced cycferation in lin D1 expre-/- mouse tucompared t

ng, implicate

alysis of HC of P2 pures P2X3 pur


nflammator

ignaling is ents with he

Randy L4; Loss, John A2

n of Gastroeational Biologe, 4Departmement of Systmunology, Bon, TX, Unit

cinoma (HCar ATP-mednd P2 purin

ologic relevaurinergic sign

expression - livers (hipere analyzed

RNA) analysiell cycle progcells expose

53 (P2X3 ant

receptor ison up to 60poor recur

d in HCC ceprogression in D3, E, aclin protein HCC cells.

ession in Huumors exhibto WT whileed in HCC pa

CC patients, rinergic signrinergic rece


32

associated epatocellula

ee, Ju-Seog2,7; Thevana

enterology, Hgy and Moleent of Biochtems Biologyaylor Collegted States.

C) is the 2ndiated activanergic recepance of purinnaling facilit

profiles (15 po-deficient d by qRT-PCs of a large

gression wased to ATPStagonist).

oforms were0% of patierrence-free ell lines. Ext

in Huh7 cnd A mRNAexpression. Interestingh7 cells, wh

bit dysregulae nucleotideathogenesis

Mst1/2-/- livenaling in theeptors as pot


Diseases in 2

with poor rar carcinom

g5; Sohn, Bonther, Sund

Hepatology &cular Medicemistry andy, UT MD Ange of Medicin

nd most letation of P2

ptors are ovenergic signatates aberra

isoforms) omice HCC

CR and immr cohort of Hs analyzed bS, ATP or A

e elevated ≥ents. High P

survival. Dytracellular ncells, as evA and prote Extracellula

gly, ATPS hich was assated expresse treatment s.

ers and HCCe induction tential new t


recurrence-ma

o Hwa5; Lopeararajah1,2,3

& Nutrition, Tine, 3Dan L. Molecular Bnderson Canne, 7Departm

hal cancer 2 purinergic erexpressedling in HCC

ant cell proli

of HCC patieC) and HCCmunohistochHCC patientby Western ADP +/- SP

≥2-fold in pP2X3 or lowysregulationucleotide trevidenced byein expressiar ATP-medtreatment i

sociated withsion of multof Huh7 ce

C cells in vitrof a hyper

targets for th

um:

-free surviv

ez-Terrada,

Texas ChildrDuncan Ca

Biology, Divincer Center,ment of Surg

worldwide. receptors

d in certain remains un

iferation und

ent livers (tuC cell lines hemistry. Fts (n=188). blotting, qR

P600125 (c-

atient liver w P2Y13 ren of P2 pureatment alony increasedion. JNK indiated activainduced a h poor progntiple P2 purells induced

ro identifies ar-proliferativeherapy.

val in

ren’s ancer sion of

gery,

Recent induce cancer known.

derlying

umor vs (Huh7, indings Impact

RT-PCR -Jun N-

tumors eceptor rinergic ne was d BrdU hibition ation of distinct

nosis in rinergic

d target

a novel e HCC

An outb

Adrienne LAttumi, Dia

Baylor ColMichael E.

The hypoththe etiologyperipheral to 50% of PCR detecmore convdisease-sporganism fwould supantibiotics.reveal a mtechniquespatients trein a villagafflicted widetection, a more covery high fand early r

Tex 6th Fron

break of IBD

L. McNees1, ane Markesic

lege of Med DeBakey V

hesis that a y of Crohn’sblood macrothese patien

ction methodvincing argupecific consifor studies o

pport unders We hypoth

more consiss viable orgeated at the e in Bahraiith Johne’s disolation and

onsistent assfrequency oresults of cul


D provides npa

Najah Zayyach3 , and Dav

icine1, BahraVA Medical C

mycobacters Disease (Cophages of nts has beends have imprument for Mistency of aof microbial

standing disehesized thatstent rate oanisms couHouston Den, which bedisease. Thd culture of sociation be

of detection lture.


nflammator

new evidenathogenesis

ani2, Fazal Tvid Y. Graha

ain SpecialtyCenter4

rium, specifCD) has been

patients withn widely reproved, labor

MAP as a cassociation, genomics, ease pathogt multiple saof detection uld be isolateBakey VA Megan recente causative MAP from

etween MAPof MAP in p


33

ce for a roles of Crohn's

Tabassam1, am1, 4

y Hospital, M

ically M. avin strengthenh CD. A posorted, but th

ratory culturecausative ag

compared molecular e

genesis andampling of p

among patted. These Medical Cently possibly agent of Jopatients wit

P and CD. Wperipheral b


Diseases in 2

e of M. avius disease

Jason Hou1

Manama, Ba

ium paratubned by the resitive MAP Phe detectione of these ogent for CDwith contro

epidemiologd an approaperipheral btients, and experiments

nter and in aafter the im

ohne’s diseah recently d

We will preslood of thes


um paratube

, 4, Antone R

ahrain2. Pulm

berculosis (Mecent detectPCR in bloo

n rate has berganisms ha

D would be ols. Further,gy, and antibach to treatblood from C

that with as are beingan “outbreakmportation oase is MAP.diagnosed Csent here ouse two CD p

um:

erculosis in

R. Opekun1,

motect, Inc. 3

MAP), has a tion of MAP od specimeneen variableas not advan

to demons cultivation biotic suscetment or cuCD patientsappropriate conducted

k” populationof a herd of We propoD will demour observatipatient popu

n the

Tariq

, and

role in DNA in

ns of up e. While nced. A strate a

of the eptibility re with

s would culture in CD

n of CD f cattle

ose that onstrate ons on

ulations

Christina MBaylor Col

In Lactobaproductionmetabolismrevealed nhistidine oror viabilitymedia whedeterminedproductionproviding bimproves hits sole soenteroids epithelium.

Tex 6th Fron

Morra and Jalege of Med

acillus reute of the pro-

m pathways o significantr 13C6

15N3 L-. While, theere all histidd that the . Together, benefit to thhistamine prource of L-hto determin. I will


L-Histidin

ames Versalicine, Houst

eri the deca-inflammatoin L. reuteri t changes inhistidine. Th

ere were no dine was re

addition ofthese data

he host, is roduction; anhistidine. Fute the effec


nflammator

ne metaboli

ovic M.D., Pon, TX

arboxylationry moleculeusing 13C6

15

n growth or vherefore, his

significant eplaced withf carnosine have demonot required

nd 3) L. reutture work w

cts of L. reu


34

ism by Lact

Ph.D.

of L-histide, TNF. We 5N3 L-histidinviability whetamine prodchanges to carnosine

e to the monstrated thd for L. reuteri strains c

will involve cuteri and hi


Diseases in 2

tobacillus r

dine to histahave begu

ne. Analysis en cultured induction is no growth or (β-alanyl-L-

medium signhat 1) histiduteri growth;can import, pco-culturing istamine me


reuteri

amine by Hun to elucida

of wild typen different c

ot essential foviability in L

-histidine), mnificantly incdine decarbo; 2) the addprocess, andof L. reuter

etabolism o

um:

HdcA reducate novel h and hdcA moncentrationor L. reuteriL. reuteri grmass spectrcreases hisoxylation, aldition of card use carnosri with human the huma

ces the istidine

mutants ns of L-growth

rown in roscopy stamine lthough rnosine sine as an ileal an ileal

Dorottya NSchady2,4, Kellermaye1Section ofTexas ChilHospital, H4Departme5Departme

BACKGROoption for treating UCin pediatricMETHODSwere stud(colonoscoimmunotheclinical anmicrobiomebacterial 1RESULTStolerated tremission. moderate tlength of cthe initiatioupon seriaCONCLUSconsideringmucosal renumber: N

Study ID

G

P001 P002* P003# P004* P005 P006# P007 P008 P009

D001

D002

A/I: Asian/Indprednisone; P(* and # indic

Tex 6th Fron

Mucosal d

Nagy-Szakal1

Milena Pitaser1,3 f Pediatric Gdren’s Hosp

Houston, TX,ent of Patholoent of Surger

OUND: Feculcerative c

C. We exploc UC patientsS: Seven paied. These

opy and reteerapy. Filterend endoscoes were ana6S rRNA ge: Patients the treatme

However, to severe sy

clinical remison of FMTs. l FMTs.

SION: Our g FMT as a emission or CT0194710

G R Eth

M W NH M W NH F W H M W NH F W NH F W H M W NH M W NH M W NH

M A/I NH

F A/I NH

dian; Eth: EthnP: pseudopolypcates the same


disease actitranspla

1,3, Emily B. shny2,4, Mon

Gastroenteropital, Housto, USA; 3USDogy& Immunry, Baylor Co

cal microbiocolitis (UC). red the clinics with mild tatients (9 tr

patients eention enemed, frozen aopic diseasalyzed by m

ene. (n=6) who nts and thesubjects w

ymptoms andssion negativ

Metagenom

findings unprimary tre

mild endosc1 (IND#1573

Age (y)

Tx prior to FMT

16 IFX 15 6-MP 14 PRED16 PRED18 PRED15 PRED20 PRED17 PRED13 PRED

37

30

nicity; F: Femap; R: Race; W:

e patient). We c


nflammator

vity may prantation in

Hollister2,4,Fica E. Lopez

logy, Departn, TX, USA;DA/ARS Chinology, Baylollege of Me

ta transplanRecent tria

cal and metao moderate reatment coenrolled intomas, Tx=37)and thawed de activities

massively pa

had endose withdrawa

with moderatd had to be vely correlat

mic stool stud

derscore thatment modcopic diseas34)

FMT specimens

D001 D001

D D001 D D001 D D002 D D001 D D001 D D001 D D001

le; G: Gender;: White; 6-MP: calculated pseu


35

redict therapediatric ul

Faith D. Ihekz5, Ruth Ann

tment of Ped 2Departmenldren's Nutrior College odicine, Texa

ntation (FMTls showed vagenomic redisease sevurses) with

o an FMT ) administerdonor stool

were moarallel pyrose

scopic remisal of their imte to severexcluded froed (r=-0.78, dies reveale

he importandality for UCse may bene

Treatment (rescue enemas)

28 (2) 25 22 32 (1) 10 17 (1) 9 2 24 (5)

H: Hispanic; 6-mercaptopu

udopolyps to ad


Diseases in 2

peutic resplcerative co

kweazu1, Abrn Luna2,4, Ja

diatrics, Baynt of Patholoition Researof Medicine,as Children’s

T) is an emvariable effiesponses to verity.

immunothetrial with ared FMTs dspecimens nitored throequencing o

ssion or mmmunotherare endoscopom the trial w p=0.013) w

ed complex

ce of mucoC. Patients wefit the most

# Mayo score before FMT 0 1 0 1 2 1 (P) 2 3 1 (P)

IFX: infliximaburine. Two patiedd 0.5 to the en


ponse to fecolitis

ria Haynes2,

ames Versalo

ylor College ogy, Texas Crch Center, HHouston, TX

s Hospital, H

merging altcacy of limiintense ser

erapy depena weaning during the wwere utilizedoughout theof the V3V5

ild mucosaapy while mpic diseasewithin 10 day

with mucosalbacterial co

osal diseasewith medicat from FMTs

Mayo score after 12 week FMT 0 0 0 0

; M: Male; NHents were enrondoscopic May

um:

cal microbio

,4, Deborah ovic2,4 and R

of Medicine,Children’s Houston, TXX, USA;

Houston, TX,

ernative treited FMT serial FMT trea

ndent pediatcourse of withdrawal od. Adverse ee protocol. regions wit

l disease vmaintaining e (n=3) devys of initiatiol disease acmposition ch

e staging pally induced s. ClincialTri

Days spentremission

261 159 105 204 10 21 9 2 58

: non-Hispanicolled twice a yeyo score.

ota

Richard

,

X, USA;

, USA

eatment eries in atments

tric UC rectally of their events,

Fecal thin the

variably clinical

veloped on. The ctivity at hanges

prior to colonic als.gov

t in

c; PRED: ear apart

Lactobac Laura OrtizDepartmen Nowadaysto the gastLactococcudisease wilimit its uscheese anATCC PTAwith any psuch as reefficiency, Regeneratsecreted toVancomycto constructherapeuticFor this puunder gastPreliminaryis secreteexpressionprotein is oloops mode

Tex 6th Fron

cillus reuter

z, Robert Brint of Molecu

, bacterial dtrointestinal us lactis areith promisingse as a thend its inabilA 6475 is a pathological combineerinmake L.

ing islet-deo the lumenin resistant ct a L. reutc tool for theurpose, we trointestinal y results shod to the e

n of Reg3α aoptimized weel of VRE .


ri as a bioth

itton lar Virology

elivery systetract (GIT)

e being expg therapeuti

erapeutic deity to survivhuman deriprocess. Th

ng and CRISreuteri a prived protei

n of the humenterococci

teri strain the treatment will engineeconditions,

ow that 95%extracellular and demonste will test th


nflammator

herapeutic s

& Microbiol

ems are a pofor therapeulored for theic effects. D

elivery systeve in some ved strain whese charac

SPR/Cas9, thpromising cain 3 alpha

man GIT, wh (VRE) and

hat efficientlyof several g

er an L. reuand will be

% of the totamedium. C

trating its anhe therapeut


36

system for

ogy, Baylor

opular tool tutic purposee treatment

Despite thesem (TDS); sgastrointes

with probioticcteristics, alhat allow preandidate fo(Reg3α) is

hich has actListeria mo

y delivers Rgastrointestinuteri strain th

used to detl produced p

Currently wentimicrobial atic effect of


Diseases in 2

the delivery

College of M

to supply reces. Lactic ac

of diseasese results, L.such as beistinal compac propertiesong with thecise manipor the delivs an antimtivity agains

onocytogeneReg3α to thenal diseaseshat approprtermine the protein is soe are workactivity in vitour TDS in


y of antimic

Medicine, Ho

combinant pcid bacteria s such as in lactis has sng a bacte

artments. La that has no

he availabilitulation of its

very of theicrobial pep

st several paes. The goale GIT and s including liriately secretherapeutic

oluble, and aking on achtro. Once thevivo by usin

um:

crobial pept

ouston, Texa

proteins or pe(LAB), part

nflammatorysome featurrium isolateactobacillus ot been assoty of genetics genome wirapeutic pe

ptide, continathogens in of our resecan be useisteriosis an

etes Reg3α effect of ou

approximatehieving a se expressionng the ligate

tides.

as.

eptides ticularly y bowel res that ed from

reuteri ociated c tools, ith high eptides. nuously cluding

earch is ed as a d VRE. in vitro

ur TDS. ely 70% suitable n of the ed ileal

MuralidharNIC1, SmriNeonatologHouston, TBaylor ColBaylor Col BackgrouThough intevolution o Objective: Design/Mefor either aover 4 weemorbiditieswas extrac16s rRNASequencinoperationa Results: 2following inNEC & peOTUs founwas assocantibiotics,infants withphylum, Slactobacillu Conclusioevenness and abundabundanceexisting inimprove ou

Tex 6th Fron

Infa

r H Premkumthi A Chakkgy, DepartmTexas, Unitelege of Medlege of Med

nd: SBS is terventions sof intestinal m

: To describ

ethods: Casa congenital eks. Controls. Stool samcted using thA gene was

g reads weal

255 stool sanfants: 4 gaserforation, 1 nd, and diveciated with and use of h complicateSBS infantsus) and grea

ons: We havof intestinal

dance decreae of Proteobtestinal mic

utcomes.


ants with shintesti

mar, MBBS, kalakal1, Josement of Peded States; 2

dicine, Housicine, Houst

a commonsuch as antimicrobiome

be the profi

ses includedor an acquirls were gestples were c

he PowerMas amplified ere analyze

taxonomi

amples werestroschisis, 5

volvulus anersity of micthe followinbreast milk

ed gastroschs showed ater abunda

ve demonstramicrobiome

ased furtherbacteria. Defcrobiome-alte


nflammator

hort bowel sinal bacteria

DCH, MRCeph F. Petro

diatrics, BayThe Alkek C

ston, Texas, on, Texas, U

cause of gbiotics and in infants wi

le and evo

d hospitalizered gastro-intational ageollected at a

ag Microbiomby PCR a

ed using thc

e analyzed f5 small intesnd 1 jejunacrobiome. Dng: birth byin comparis

hisis and NEdecreased

ance of Prot

ated that infe. Significanr when assofining the intering therap


37

syndrome (al richness

CPCH1, Nadiosino, PhD2

ylor College Center for MUnited Stat

United State

gastrointestiprobiotics arth SBS is un

lution of in

ed SBS infanntestinal cone-matched hoa weekly inteme isolation and sequene QIIME, a

unit

from 16 casstinal perforal atresia. Caecreased di

y Cesarean son to formuEC demonstr

abundanceteobacteria

fants with SBntly, within thciated with ctestinal micrpies and pro


Diseases in 2

(SBS) have and divers

im J. Ajami,and Brendaof Medicin

Metagenomictes and 3 Mo

es.

inal mortalitre commonlnknown.

testinal mic

nts who undndition, and rospitalized ierval, till diskit (MoBio)

nced on thand the SIL

(OT

ses and 21 ations, 1 necases showeiversity thousection, ab

ula when orarated the leae of Firmi(Pseudomo

BS have deche group ofcomplicationrobiome in inomote deve


decreased sity

PhD2, Paman Lee, MD, ne, Texas Ccs and Microlecular and

ty and morby used in SB

crobiome in

derwent a surequired parinfants withocharge fromand the bac

he MiSeq (LVA databaTU)

controls. Ccrotizing ented both decugh not statbsence of oally fed. Withast diversity.ictues (lach

onas and Esc

creased richf SBS, the dns. SBS gronfants with Selopment of

um:

mela GordonPhD3. 1 Div

Children's Hrobiome Resd Human Ge

bidity in neoBS, the natu

infants wit

urgical intervrenteral nutriout gastroin

m the hospitacterial V4 reIllumina) plase was us

classif

Cases includterocolitis (Ncreased amoistically signoral feeds, hin the SBS. At the levehnospiraceacherichia-Sh

ness, diversdiversity, eveup showed SBS, will ref

new strate

, RNC-ision of ospital, search, enetics,

onates. ure and

th SBS

vention ition for testinal

al. DNA egion of atform.

sed for fication.

ded the NEC), 4 ount of nificant, use of group,

el of the ae and higella).

sity and enness greater fine the gies to

Caná RosPetri Urvil1

Savidge1,2 Baylor ColBranch3, U Clostridiumhealth probetween thmechanismpatients wmetabolomaminobutypredictive difficile toxwith closeluminal GAdifficile. In CDI pathog

Tex 6th Fron

The role

s1,2, Alex P1,2, Mathew

llege of MedUniversity of

m difficile is oblem for hhe disruptionm of CDI suswho developme signatureric acid (GAof disease s

xin virulenceely related ABA potentiasummary, e

genesis and


e of GABA i

Peniche-TrujPena5, Geo

dicine1, TexaHouston - S

a leading caospitals ann of the gut sceptibility a CDI have

es that are fABA). Elevasusceptibilitye via activatiGABA-produated microbielevated mic represents


nflammator

in susceptib

illo3, Michaerge Bennett

as ChildrensSchool of Pha

ause of nosd long-termmicroflora a

and recurrensignificant

unctionally aated stool Gy in patientson of GABAucing Clostial dysbiosis

crobial GABAa novel dise


38

bility to Clo

el Loeffelhot5, Hoonmo

s Microbiomarmacology4

socomial infem care faciliand the devence is not wantibiotic-asassociated wGABA and and in expe

A receptor Atridial spp. s during CDA productionease target f


Diseases in 2

ostridium di

lz3, SamuelKoo1, Kevin

me Center2, 4, and Rice U

ection in theities. Despielopment of ell understossociated shwith increaszolpidem u

erimental CA signaling.

Further invI and increa

n constitutesfor therapeut


ifficile infec

l Aitken4, Nn Garey4, Sa

University oUniversity5

e U.S. and rte an estab

f C. difficile iood. Here wehifts in stoo

sed L-argininuse (a GABDI models, Stool GABA

vestigation dased mucosas a significantic interventi

um:

ction

Numan Oezgara Dann3 a

of Texas - M

represents ablished corrinfection (CDe demonstraol microbiomne conversioBAeric drugand potentiaA levels cordemonstrateal adherenc

nt new risk faion.

guen1,2, and Tor

Medical

a major relation DI), the ate that me and on to -g) were ated C. rrelated ed that ce of C. actor in

E JS Schaefe Departmenat Houston Backgrouand acetylepigenetic However, known. Fu(IL-10) andchildren. Tintestinal homeostasa RING finplayer in tdistinct epiexamine thepigenetic Methods Uintestinal inwas used mucosal tis Results Cubiquitylatiubiquitylate Conclusioand suggethat a lackthat may co This work the Crohn'developme

Tex 6th Fron

Epigenetic a

er, H Howor

nt of Diagnosn School of D

nd Epigeneation, contri

modificatiothe contri

urther, recend the IL-10 Taken togethinflammation

sis. In concenger ubiquitithe IL-10 reigenetic marhe epigenetprofile of Rc

Using the ILnflammationto obtain a

ssue and ce

ChIP analysion in the ILed in BALB/c

on Our data est a fundamk of IL-10 sigontribute to

has been sus & Colitis F

ent grant.


and transcr

rth, N Nakra,

stic and BiomDentistry. Ho

etic modificabute to the

ons have bbution of

nt next-genereceptor ge

her with then, it is cleert with thesn ligase with

egulatory parkers may dtic markers c3h1 in muc

L-10-/- mousn. In these sa detailed plls of IL-10-/

is revealed L-10-/- micec mouse mu

indicate thamental role fognaling, as colitis.

upported by Foundation o


nflammator

riptional reg

, D Montufar

medical Scieouston, TX, U

ations, exemregulation o

been assocepigeneticsration seque

enes that ase IL-10 knoear that IL-e observatioh immune m

athway. Giveemarcate inassociated

osal biopsie

se model, wstudies, chrorofile of me/- mice.

that the Rce. In contrasucosal biops

t the Rc3h1or Rc3h1 in evidenced i

NIH grants of America’s


39

gulation of i

r-Solis, N Vig

ences, The UUSA, 77054

mplified by Dof gene expriated with

s to inflamencing analyssociate withckout (IL-10-10 signalinons, our premodulatory aen this comndividuals th

with defeces from IL-10

we examinedomatin immuethylation an

c3h1 locus st, the Rc3hies.

locus is tranmucosal im

n the IL-10-

DK035566 as (CCFA) an


Diseases in 2

inflammatio

gneswaran,

University of4.

DNA methylaression. Abndisease pr

mmatory boyses uncoveh early onse0-/-) mouse ng is essenevious studieand RNA sta

mplex etiologhat are predictive IL-10 s0-/- mice.

d the epigeunoprecipitand acetylatio

had increah1 locus is

nscriptionallmmune home-/- mice, has

and by a Cand an Institu


on in IL-10-/

and JR Klei

f Texas Hea

ation and hnormalities inrocesses, powel diseasered mutationet of ulceramodel that

ntial to maes identified ability functiogy of IBD, wisposed to dsignaling, w

netic markeation (ChIP) on at the R

sed methylapoorly meth

y silenced deostasis. Ths significant

areer Develoution-funded

um:

/- mouse

in.

alth Science

histone methn these patt

particularly cse (IBD) ins in interleu

ative colitis (t develops caintaining m

Rc3h1 (Roqons, as a powe postulatedeveloping I

we investigat

ers associatefollowed by

Rc3h1 locus

ation and rehylated and

during inflamhey further it epigenetic

opment Awa CCTS/K12

Center

hylation terns of cancer. s less ukin-10 (UC) in chronic

mucosal quin-1), otential ed that BD. To ted the

ed with y qPCR in the

educed d highly

mmation ndicate effects

rd from career

Tattym E. SBaylor Col More than this year. current treetiology oftransformaperinuclearestricted bWe develoand we fouis almost demonstraoncoproteithe translowas shownperinucleusthe regulattransmissioproperties On the bastructurallyregulates pnew therapappears hithe perinuccolon caninflammato

1. Len

can2. Wa

PM3. Wil

and4. Koc

Cro200

5. Xiaaccnet

6. Sha201

Tex 6th Fron

Ch

Shaiken andlege of Med

fifty thousaIt is estimat

eatments aref malignant tations1 manyr viral accumby the absenoped an isolaund that it cohalf of the

ated that the n, Ras, prev

ocation of then to correlates. We showtion of proteon electron of the perinusis of our re

y dynamic protein biosypeutic targeghly importacleus, descr

ncer biologyory bowel dis

ngauer C, Kincer cells. Pang D, Dubo

MID:2016831liams CS, M

d developmechs G, Janzeosse virus nu02; 99:3153-o PJ, Samu

cumulation owork. J Viroaiken TE, Op14; 4:4923.


haracterizat

d Antone R. icine – Gast

nd men andted that onlye most liketransformatiy of which mmulation.4,5 nce of any isation techniqontains apprproteins of perinucleus

viously ascrie p53 tumore with the trawed that theein biosynthe

microscopucleus. esults, the corganelle. ynthesis, ap

ets. Investigant in the unribed hereiny, possibly sease and b

nzler KW, VProc Natl Acais RN. Eico9

Mann M, DuBent. Oncogeen C, Hohenucleocapsid -8. PMID:11lski RJ. Cyt

of adeno-assol. 2012; 86:pekun AR. PMID:24815


nflammator

ion of the p

Opekun, Jr.troenterology

d women in y about 4 ofly to be suon is enigm

may be propaUntil now, a

solation methque on the broximately 1nuclei.6 U

s’ compositioibed to the pr-suppressoranslocation

e rate of fastesis in the py and deco

concept of tTaken tog

ppears to cogation of thenderstanding, may open

including biliary atresia

Vogelstein B.ad Sci U S Asanoids and

Bois RN. Thene. 1999; 1nberg H, Haprotein into

1880649 toplasmic trasociated viru:10462-73. PDissecting th5916


40

perinucleus

y Sections

the U.S. wilf 10 cases w

uccessful, anmatic, but ap

agated by cn investigatihod. asis of the p7% of the tosing four dion is highly plasma memr protein to tof p53-stabit- and slow-perinucleus,onvolution

he perinuclegether, the ontribute to ge role of theg of colon ca

up broad, nhepatocellu

a.

. DNA methA. 199; 94:25d cancer. Na

e role of cyc8:7908-16. ller O. Antivperinuclear

afficking, ends type 2 parPMID:22811he cell to nu


Diseases in 2

in colon ca

l prematurewill be diagnnd better a

ppears multi-chronic inflamion of the ro

perinucleus’ otal proteinsifferent normdynamic. In

mbrane, andthe perinuclilizing proteigrowing colo but not in microscopy

eus is advaperinucleus

gene exprese perinucleuancer progrenew researclar carcinom

hylation and 545-50. PM

at Rev Cance

clooxygenasPMID:1063

virally active complexes.

dosomal escrticles are fa1523 ucleus, perin


ancer cells

ly succumb nosed at an pproaches -factorial anmmatory conole of the per

unique, coms of the mammal and cann this fractio

d Src onocopeus in immoin, nucleophon cancer cthe cytoplasconfirmed

nced as a fs maintains ssion and pus in malignession. The ch opportunima, Barrett

genetic instaMID:9122232er. 2010; 10

ses in inflam0643 MxA protein

. Proc Natl A

cape, and peacilitated by m

ucleus and

um:

from colon early stage

are needednd includes gnditions,2,3 srinucleus ha

mpact organmmalian cellncer cell linon we detecprotein. Moortalized MEhosmin (B23cells dependsm. Applica

distinct str

formal, idennuclear in

points to potnant transfor

characterizaties that trat’s transform

ability in colo2 0:181-93.

mation, can

n sequestersAcad Sci U S

erinuclear microtubule

cytosol. Sci

cancer e, when d. The genetic

such as as been

ization, , which

nes, we cted the oreover, EF cells ) to the

ds upon ation of ructural

tifiable, ntegrity, tentially rmation ation of nscend mation,

orectal

cer,

s La S A.

i Rep.

Reu

Jennifer K.Runge1,2, E

1Texas ChBates AveMedicine, Oof MedicinAdministra

Backgroudifficile. Uphospitals amicrobiota understandantimicrobof therapeu

Results Mabundancedeveloped antibiotics vancomyciwhich are mutant strReuterin (pdu-cbi-heglycerol is FurthermoC. difficile and patieunappreciae.g. surfacL. reuteri targeting m

ConclusioabundanceLactobacillresistant scommunityCDI. As antimicrobtreatments

Tex 6th Fron

uterin – Inve

. Spinler1,2, , Emily B. Hol

hildren’s Mice., Houston,One Baylor ne, One Baation, Univers

nd The mosp to one milapproachingand the de

ding of how ial defense mutic inhibitor

Metagenomie of Lactob

a recurrenmaking thisn (MIC 256 commonly u

rains unable3-hydroxypr

em-cob clusthighly effecre, administexpansion, p

ents. Using ated posttrance protein Sland glycero

microbial infe

ons Metagene of Lactobalus ssp. knowtrain with g

y analysis in part of a

ial mechans for CDI.


estigation o

Jennifer Aulister1,2, Jam

crobiome Ce, TX, USA;Plaza, Housaylor Plazasity of Houst

st prolific callion cases a

g 40%. Development ohost bacterimechanism s currently b

c analysis bacillus sspnt episode. s a resilientg/mL), fida

used in CDIe to producropionaldehyter and glyctive and seleration of eithproviding str

mass spenslational mpA. Finally,

ol administraection.

nomic analyacillus spp. inwn to be safreater cytotoa bioreactoDDC Pilot ism, and t


nflammator

of a novel s

chtung3, Tomes Versalov

enter, Depar 2Departme

ston, TX, US, Houston, ton College

ause of bacare reported

espite a knoof symptomsa protect agtargeting C.

being develo

of stool s. to be sig

As a gent treatment axomicin (M therapy. C

ce the antimyde) produccerol. We dective againher glycerol rong justificaectrometry, odifications we demons

ation, allowi

ysis of stool n patients wfe in humansoxicity to C.r supported Award, we o exploit th


41

signaling me

ny Haag1,2, Avic1,2,3, Kevin

rtment of Paent of PathoSA; 3Molecul

TX, USA; of Pharmacy

cterial-induced annually aown inverses in infectedainst this pa difficile, wh

oped to treat

pecimens fgnificantly dus, Lactobaoption for CIC >32 g/m. difficile gro

microbial, rection by L. rdemonstratednst C. difficile

or purified ration for usin

we demoof target pro

strated C. ding developm

specimens with recurrent

s. We ident. difficile thaL. reuteri anaim to ch

his novel f


Diseases in 2

echanism in

Aaron Brown Garey4, Ro

athology, Teology & Imar Virology &

4Departmey, Houston,

ed diarrhea at a cost >$e correlationd patients, thathogen. Weich functions

t CDI.

from CDI pecreased inacillus spp. CDI. ParticumL), and metowth in vitroeuterin, do reuteri requd that the ce in a humareuterin alonng L. reuterionstrate thaoteins that aifficile killing ment of a p

from CDI pt disease, wtified L. reutean vancomynd glycerol aharacterize tfinding to d


n gut-micro

wn1,2, Ruth Anobert A. Britt

exas Childremmunology,

& Microbioloent of Clini

TX, USA

in the U.S.$3.5 billion, wn between here is still ae have idents as the phy

patients shon patients w

are intrinsularly, L. reutronidazole (

o is inhibitednot inhibit C

uires the hocombinationn microbiota

ne to bioreaci and glyceroat reuterin are vital for in the gut lu

prototypic th

patients revewhich led us eri as an int

ycin and fidaas a potentiathis previoudevelop pro

um:

obial health

nn Luna1,2, Jton3, Tor Sav

en’s HospitaBaylor Coll

ogy, Baylor Ccal Science

. is infectionwith rates inthe protectia major gaptified a new,ysiological co

owed the rwho subseq

sically resisuteri is resis(MIC >256

d by L. reuteC. difficile g

orizontally acn of L. reutea bioreactor ctors did notol in animal

forms preC. difficile sumen followiherapeutic c

ealed a decto screen prrinsically anaxomicin. Mal therapy tausly unappreototypic adj

Jessica vidge1,2

l, 1102 ege of

College es and

n by C. n some ive gut

p in our , potent orollary

relative quently tant to

stant to g/mL), eri, and growth. cquired eri and model. t inhibit models

eviously urvival, ing oral concept

creased robiotic tibiotic-icrobial

argeting eciated unctive

Ablation

Xiaojun Ma Children’s Houston, T

Adipose insyrup (HFCSome sturesistance,HFCS concompared with 8% Hconsumed HFCS-fed intake andpathogenetriggered aATMs (F4/less abundpromoting hormone sresistance beyond theoption for p

Support: 12IRG9230Award #1-

Tex 6th Fron

n of ghrelin

a, Ligen Lin,

Nutrition RTX, USA

flammation CS) is the mdies have , while otherntinues to bthe metabo

HFCS in drthe most camice exhib

d body fat cesis of obesia robust incr/80+CD11c-) dant in HFCadiposity a

secretagogueand liver s

e calories apreventing/tr

USDA/CRIS0004 and 115-BS-177 (


receptor atinfl

Geetali Pra

Research C

and insulin rmost-used sw

suggested rs are in dis

be used as lic effects ofrinking watealories, and

bited most scontent. Adipity and insurease of botin visceral f

CS-fed miceand insulin e receptor (Gsteatosis. Thassociated wreating inflam

S grant AR4GRNT1899

(YS).


nflammator

ttenuates hiammation a

adhan, Huaiz

enter, Depa

resistance pweetener in

that HFCSagreement. the primary

f mice fed reer (to mimic

showed thesevere insulpose tissue lin resistancth pro-inflamfat. Remarkae than in hiresistance. GHS-R) amhus, HFCS

with it, and Gmmation and

RS3092-5-090019 (YS)


42

igh fructoseand insulin

zhu Wu, C. W

artment of

play causal rthe United S

S consumptDue to con

y sweeteneregular diet, hc soft drinke highest wein resistancmacrophag

ce. Here wemmatory ATMably, howeveigh fat-fed mWe found

eliorates HFconsumptio

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01-059 (YS, and Amer


Diseases in 2

e corn syruresistance

Wayne Smit

Pediatrics,

roles in type States, substion correlatflicting and r in our foohigh fat diet

ks). As expeight gain ance, which wges (ATMs) e show that Ms (F4/80+Cer, the anti-imice. Ghrelthat deletio

FCS-inducedon has detragonists maistance.

S), Americarican Diabet


up (HFCS)-in

h, Yuxiang S

Baylor Col

2 diabetes. stantially reptes with obinsufficient s

od supplies. t, or regular ected, highnd fat depos

was dispropoplay an imsimilar to h

CD11c+) andnflammatorylin is an oreon of ghrelid adipose inrimental effeay represent

an Heart Ates Associat

um:

nduced adip

Sun

llege of Me

High fructosplacing tablebesity and scientific ev

In this studiet supplem fat diet-fedsition. Surprortionate to portant role

high fat diet;d anti-inflamy ATMs wereexigenic hon receptor flammation,

ect on metat novel thera

Association tion Basic S

pose

edicine,

se corn e sugar.

insulin idence, dy, we mented d mice risingly, calorie

e in the HFCS

mmatory e much

ormone, growth insulin

abolism apeutic

grants Science

Obeti

Tessier, MSara3; FranSavidge, T

1. PediatricTX, United2. Patholog3. Internal 4. Biology,5. Virology

Backgroutherapy forecurrencetreatment (FXR), a bimportant analogue Methods: mouse CDvitro, we ason spore Results: OVPI1640 oafter 48 huninfected mice, suggwhere INT-[Ki for CDCgrowth in t

Conclusiodiseases a747 as preand growththerapeutic

Tex 6th Fron

icholic acid

ary Elizabetncis, Michae

Tor2

c Gastroente States. gy, Texas CMedicine, In Texas A&M

y and Microb

nd: Clostridr C. difficile

e rates, andoptions are ile acid recerole in C. dand potent

The clinical DI disease mssessed the

germinatio

Oral INT-74or NAP1 C. hr, INT-747

mice. Surpgesting that -747 inhibite

CA 131 + 10 he low µM ra

on: INT-747as well as inseventative thh. With currc tool in the f


d (INT-747) c

th M.1; Andeel4; Sorg, Jos

erology, Bay

hildren's Honfectious Dis

M, College Stbiology, Bayl

dium difficile infection (C

d newer, tatherefore g

eptor, is knodifficile virult FXR ago

efficacy of dmodel using e INT-747 mon of C.

47 demonstrdifficile spotreated ani

prisingly, INTit may dire

ed spore gerµM vs 215

ange.

is currentlsulin resistanherapy for Crent FDA fasfight against


nflammator

confers disein

rsson, Helenseph4; Theva

ylor College

spital/ Baylosease, UTMBtation, TX, Uor College o

is the leadinCDI) is avairgeted antibgreatly needown to ameli

ence. Thusonist obetic

daily INT-747wild type C

inimum inhibdifficile VP

rated good res. Whereamals maintaT-747 exerteectly target rmination wit+ 46 µM for

y receiving nce. Here w

CDI, via direst-track dest C. difficile.


43

ease protecfection.

n2; Ross, Caananther, Su

of Medicine/

or College ofB, Galveston

United Statesof Medicine,

ng cause oflable, convebiotics can ded for this orate intesti

s, we investholic acid

7 (10-50 mgC57bl and Fbitory conce

PI1640, 630

clinical effias vehicle trained a based a similarC. difficile. th similar poINT-747.] F

much attewe demonstra

ct inhibitory ignation, INT


Diseases in 2

ction agains

ana2; Penichundararajah

/ Texas Chil

f Medicine, Hn, TX, Unites. Houston, TX

f bacterial dentional drugalso result serious disnal inflammtigated whe(INT-747)

g kg-1 day-1) wFXR (-/-) genentration as w0 and clin

cacy in C5reated animseline weigr protective This was c

otency to cheFurthermore,

ention as a ate a novel oaction on C

T-747 may


st Clostridiu

he-trujillo, Aleh1; Conner, M

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chesneau1, J

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44

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n secreted rous functiohibiting glucgs are currecurrent formuobiota playserolemia andwn to alteoting GLP-1obesity. Thetimulate GLProm human

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cells which lg insulin sec

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Hongtao W 1DepartmeImmunologPerelman SPhiladelphNutrition, B *These aut Although mneurons reand the HGMET are eenteric neuvanishinglyincluded inkinase (PIlength as dpeptide (Cintrinsic prdomain (Mdeformatioloss of MEextracellulacell proliferesults sugIPANs andresponse t

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ent of Pediatgy, WashingSchool of Mia, Philadelp

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did MEK inhiCGRP) immurimary affereMetfl/fl; Wnt1on, but not inET-IR neuritear domain. ration compggest that Hd that theseo bowel inju


rt mouse end intestinal e

arina Avetis

rics, 2Departton Universiedicine at thphia, PA; 4Dege of Medici

buted equally

ic neuron sy understoodr MET mightn the fetal antiation and ounts (1 pga. HGF effers and by Mibitor. In aduunoreactive ent neurons Cre+ mice)

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yan1,2*, Rob

tment of Devity School ofhe Universityepartment one, Houston

y to this wor

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o radial musyenteric plextfl/fl; Wnt1CreT animals afignaling is ially regulate


45

ous system roliferation

bert O. Heuc

velopmentalf Medicine, Sy of Pennsylvf Pediatric G

n, TX.

rk.

e known, fad the hypothme types ofteric nervouth when add

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l Biology, 5DSt. Louis, MOvania and th

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Department oO; 3Departmhe Children’sology, Hepat

ding trophicepatocyte gurons and foENS). In vitred ENS prerotrophic facked by phonhibitors alsubset of calcplexus that g mutation alsis in resutation also ntibody to thel injury andlfate (DSS)

ment and fund epithelial c

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Purpose: several mainduced cowhich COXCOX-2, waTNBS.

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Conclusioinhibiting tThis suggeinhibitors.

Tex 6th Fron

Perfusion wt

Song Gao, M

nt of PharmaStreet, Univ

The cyclooalignancies iolitis in rat cX-2 is substas assessed

30mg TNBS12 hours la

d and perfusSO) or 0.1, anus per 2s. The conteraphy-tandeolon tissue.

he concentran rate couldwith blank HBups perfuse03 and 0.0n was 156±427±36, 70±110μM celec

and P<0.000

on: Perfusionthe activity oests that this


with celecoxrinitrobenze

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acological anversity of Hou

oxygenase-2ncluding col

colon is frequtantially indud for its effe

in 200μL 5ater, the ratsed with 0.51 and 10μM

20 minutes ents of prostem mass sp

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pectrometer

GE2 in the pepriately descenuation rat1 and 10μ

in-1, respece in the grou±4min, respecantly decreively).

coxib decelen inflamed rfusion mode


46

ates the ratec acid (TNB

eutical Scienston, TX 770

protein is ocer (CRC). 2as a model

s study, celeX-2 activity in

l was adminesthetized ank's balance(n=4~6 for es and then 2 (PGE2) in t

(LC-MS/MS

erfusate decrcribed by a te constant KM celecoxib

ctively. In thups perfusedectively. Coased the ha

rated the PGrat colon, anel may be us


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nces, Colleg030, USA

often expres2,4,6-Trinitrol for inflammecoxib, a sen rat colon

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K was deterb, K was dehe control d with 0.1, 1mpared with

alf-life of PG

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production rat colon

ge of Pharma

ssed in inflaobenzenesulmatory boweelective and with inflamm

the colon oments of prtion (HBSS)). The perfuted by solidrate were dendicator of

ng the perfuequation. In mined to beetermined togroup the and 10μM h the controE2 attenuatio

tion in TNBSct is concenvo screenin

um:

in 2,4,6-

acy, 1441

amed tissuelfonic acid (T

el disease (Ipotent inhi

mation indu

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usion period the control

e 0.005±0.00o be 0.006±half-life of celecoxib th

ol group, peon in the pe

S-induced contration-depeg model of

es and TNBS)-BD), in bitor of ced by

Dawley n were vector

ollected traction y liquid tivity in

and its l group

01min-1. ±0.002, f PGE2 he half-erfusion erfusate

olitis by endent. COX-2

Feeding

Yuying LiuDepartmen 2Allergy/ImScience Ce Backgrouinflammatolevels of effector/mecells modudriven autodysregulatlymphoproWhen we MechanismAims: To mucosa, spMethods: C57BL/6J the offsprinscurfy phewas recognisolated froanti-CD4/Cby flow cycultured anpresence oPMA/Inom(Th17) andResults: Sin intestinathe expansSystemic acontain a hreduced thproinflammLR17938 tdirectly inhConclusiodemonstraTh1/Th17 human aut

Tex 6th Fron

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fed LR17ms by which determine ifpleen and peScurfy mic

normal maleng will be he

enotype (scanized, mice om ileum, mCD44 to lookytometry. Nnd induced tor absence oycin with b

d analyzed bSf mice showal mucosa csion and actanti-inflammhighly expanhe number

matory IL17Ao sf mice de

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illus reuteri effe

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uteri DSM models of nea TLR-4-deulatory T (Trultiple immue Scurfy, sf hy, enteropd severe mmice by g

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47

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ric Researchouston, TX 7

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sed activateOral feeding and inflamma938 were alsvated CD4+Trtantly, in ccreased in Lof CD4+T an and Th17 cflammatory

activation ofe of Foxp3+Tes.


Diseases in 2

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e changes acibits Th1/Thirs of Foxp3xp3 gene is on (sf). Male rowth) on D by gavage,

ens and peripD45Rb to qupleen of wildadding spec. After 5 daCD4, intrace

d CD4+T ceLR17938 to

atory Tem cso observed

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f CD4+T ceTreg cells. L


systemic ane

nd J. Marc R

he UniversitA

s been shoNEC), assoc

while differeintestinal mu

f Tregs causwith IPEX smice gene on day of was signif

not been invctivated CD417 differenti3sf heterozyon the X chrsf mice genOL 13-15. O daily for 7 dpheral blooduantify inflamd-type (wt) cific cytokineys, cells we

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lls and inflamo sf mice sig

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Rhoads 1,3

ty of Texas

own to havciated with reentially moducosa. Foxpses lethal, Csyndrome (Imerally die f life (DOL) ficantly incr

vestigated. 4+T cell in ination. ygous femaromosome, nerally deveOnce sf phedays. Immund were labelmmatory Temice were

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mmatory Tegnificantly rentestine and e. Sf spleneeding of LRhe percentan addition, fral blood. LRcells in vitro7938 were ir differentiaay be benef

atory

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e anti-educed dulating p3+Treg CD4+T-mmune

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nocytes R17938 ages of feeding R17938 . shown,

ation to icial for

ShaiGraUT shai

JessiPostMDbow

Hashem El-SDirector Baylor Colleghasheme@bc Mary K. EsteDirector EmeBaylor Collegmestes@bcm Lenard M. LicAssociate DirDirector, InteUniversity of Lenard.M.Lic Lopa Mishra, Associate DirMD Andersolmishra@mda Douglas BurrAssociate DirBaylor Collegdburrin@bcm Milton FinegoDirector, CellMorphology CBaylor Collegfinegold@bcm

ilesh Advani, Maduate ResearcHealth Scienc

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Michael MancinCo-Director, CMorphology CoBaylor College mancini@bcm Cecilia LjungbeAssociate DirecMolecular MorBaylor College [email protected] James VersalovDirector, FunctProteomics CoBaylor College [email protected] Lisa White, Ph.Co-Director, FGenomics & PBaylor College [email protected] Joseph PetrosinAssociate DirecGenomics & PBaylor College jpetrosino@bc

LIST OF Phabet ica l o

oseph Alcorn, ssociate ProfeT Health Scie

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helcy BrumlowGraduate Studeam Houston Sbrumlow@shs


48

C LEADER

ni, Ph.D. Cellular & Molecore of Medicine .edu

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vic, M.D., Ph.Dtional Genomic

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Karen Uray, Ph.Associate DirectBiology Core University of TeKaren.L.David@

David Y. GrahamCo-Director, DDDirector, Study D& Clinical ReseaBaylor College odgraham@bcm.

Fasiha Kanwal, MCo-Director, StuClinical ResearchBaylor College [email protected]

Center ContactSara M. TristanTMC DDC AdTel: 713-798-2Fax: 713-798-0escamill@bcm

ast name.)

Jennifer BaileyAssistant ProfUT Health SciJennifer.M.Bai

Robert Bryan,Professor and Baylor [email protected]

um:

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of Medicine edu

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exas Medical [email protected]

m, M.D. DC Design arch Core of Medicine .tmc.edu

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scar Chavez, Bsearch Assistam Houston [email protected]

mothy Cifelli, raduate Studenylor College o

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[email protected]

retchen Diehl,sistant Profesylor College oetchen.diehl@

ashem El-Serahief, Gastroentylor College osheme@bcm.

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eorge Ferry, Mofessor Emerixas Children'[email protected]

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Yanna Cao, MAssistant ProfUT Health SciYanna.Cao@u

Min-Shan CheStudent Baylor Collegeminshanc@bc

Sean Colgan, PSymposium SpeaDirector of MuProgram, UnivSean.Colgan@

eanette CriglaPostdoctoral ABaylor Collegec044649@bcm

Anna Mae DieExternal AdvisoDigestive DisoDuke Universiannamae.diehl

Charles Elson,Symposium SpeaProfessor University of Acoelson@uab.

Khalil EttayebSenior Staff ScBaylor Collegeettayebi@bcm

Milton FinegoInternal AdvisoryChief EmerituTexas ChildrenMJFINEGO@


49

MD fessor ience Center auth.tmc.edu

en, M.S.

e of Medicinecm.edu

PhD aker ucosal Inflamversity of Colo

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Member ist

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Jeanette CarlsResearch AssSam Houstonjmc079@shsu

Bruno ChumAssistant ProBaylor Collegchumpita@b

Margaret ConAssociate ProBaylor Collegmconner@bc

Sara Dann, PAssistant ProUniversity ofsmdann@utm

David DurgaInstructor Baylor Collegdurgan@bcm

Melinda EngPost-doctoraBaylor Collegmelinda.enge

Nicole FatheResearch UT Health Scnicole.fathere

Roberto FlorProgram DireNational Canflores2@mail

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mpitazi, MD ofessor ge of Medicinebcm.edu

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hunxu Gao, Phraduate studenylor College [email protected]

regory Guthriestdoctoral Felylor College [email protected]

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T Health Scienudrey.Hendley

mily Hollister, sistant Profesylor College [email protected]

seph Hyser, Phsistant Profesylor College oeph.hyser@b

Jiao, MD sistant profesylor College [email protected]

anreet Kaur, Mmposium Speakesistant Profesylor College oanreet.Kaur@

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Loning Fu, PhAssistant ProfBaylor Collegeoningf@bcm.

David Y. GrahInternal AdvisoryProfessor Baylor Collegedgraham@bcm

Anne Hall, MSGraduate StudTexas [email protected]

Girish HiremaClinical FellowTexas Childrenhiremath@bcm

Hillary HoworResearch AssisUT Health SchHhoworth@ca

Faith IhekweaPediatric GastBaylor Collegefaith.ihekweaz

Coreen JohnsoPostdoctoral RBaylor Collegecoreenj@bcm

Richard KellerSymposium OrgaAssistant ProfTexas Childrenkellerma@bcm


50

hD fessor e of Medicine.edu

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Robert Fultz,Graduate StuBaylor [email protected]

Rick Guan, PAssistant ProBaylor Collegxguan@bcm.

Baokun He, PPostdoc FelloUT Health Scbaokun.he@u

Kendal HirscProfessor Baylor Collegkendalh@bcm

Diane HutchPredoctoral FBaylor [email protected]

Yanjun JiangResearch AssBaylor Collegyanjunj@bcm

Lina Karam, Assistant ProBaylor Colleglbkaram@bcm

Sunkuk KwoAssistant ProUT Health Scsunkuk.kwon

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