CCL25CCR9 Interactions Regulate Large Intestinal Inflammation in a Murine Model of Acute Colitis 英文参考文献.docVIP

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CCL25CCR9 Interactions Regulate Large Intestinal Inflammation in a Murine Model of Acute Colitis 英文参考文献.doc

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CCL25CCR9 Interactions Regulate Large Intestinal Inflammation in a Murine Model of Acute Colitis 英文参考文献

CCL25/CCR9InteractionsRegulateLargeIntestinal InflammationinaMurineModelofAcuteColitis Marc-AndreWurbel1*,MariaG.McIntire2,PeterDwyer1,EddaFiebiger1* 1DivisionofGastroenterologyandNutrition,Children’sHospitalBoston,andDepartmentofPediatrics,HarvardMedicalSchool,Boston,Massachusetts,UnitedStatesof America,2DepartmentofPathology,HarvardMedicalSchool,BrighamandWomen’sHospital,Boston,Massachusetts,UnitedStatesofAmerica Abstract Background Aims: CCL25/CCR9 is a non-promiscuous chemokine/receptor pair and a key regulator of leukocyte migrationtothesmallintestine.WeinvestigatedherewhetherCCL25/CCR9interactionsalsoplayaroleintheregulationof inflammatoryresponsesinthelargeintestine. Methods:Acuteinflammationandrecoveryinwild-type(WT)andCCR92/2micewasstudiedinamodelofdextransulfate sodium(DSS)-inducedcolitis.Distributionstudiesandphenotypiccharacterizationofdendriticcellsubsetsandmacrophage wereperformedbyflowcytometry.Inflammatoryboweldisease(IBD)scoreswereassessedandexpressionofinflammatory cytokineswasstudiedatthemRNAandtheproteinlevel. Results:CCL25andCCR9arebothexpressedinthelargeintestineandareupregulatedduringDSScolitis.CCR92/2miceare moresusceptibletoDSScolitisthanWTlittermatecontrolsasshownbyhighermortality,increasedIBDscoreanddelayed recovery.Duringrecovery,theCCR92/2colonicmucosaischaracterizedbytheaccumulationofactivatedmacrophagesand elevatedlevelsofTh1/Th17inflammatorycytokines.Activatedplasmacytoiddendriticcells(DCs)accumulateinmesenteric lymphnodes(MLNs)ofCCR92/2animals,alteringthelocalratioofDCsubsets.Uponre-stimulation,Tcellsisolatedfrom theseMLNssecretesignificantlyhigherlevelsofTNFa,IFNc,IL2,IL-6andIL-17AwhiledownmodulatingIL-10production. Conclusions:OurresultsdemonstratethatCCL25/CCR9interactionsregulateinflammatoryimmuneresponsesinthelarge intestinalmucosabybalancingdifferentsubsetsofdendriticcells.Thesefindingshaveimportantimplicationsfortheuseof CCR9-inhibitorsintherapyofhumanIBDastheyindicateapotentialriskforpatientswithlargeintestinalinflammation