Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to Clostridium difficile 英文参考文献.docVIP

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Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to Clostridium difficile 英文参考文献.doc

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Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to Clostridium difficile 英文参考文献

ModelingtheRoleofPeroxisomeProliferator-Activated ReceptorcandMicroRNA-146inMucosalImmune ResponsestoClostridiumdifficile MonicaViladomiu1,2,RaquelHontecillas1,2,MireiaPedragosa1,2,AdriaCarbo1,2,StefanHoops1,2 PawelMichalak4,5,KatarzynaMichalak4,RichardL.Guerrant2,3,JamesK.Roche2,3,CirleA.Warren2,3 JosepBassaganya-Riera1,2 , , * 1NutritionalImmunologyandMolecularMedicineLaboratory,VirginiaBioinformaticsInstitute,VirginiaTech,Blacksburg,Virginia,UnitedStatesofAmerica,2Centerfor ModelingImmunitytoEntericPathogens,VirginiaTech,Blacksburg,Virginia,UnitedStatesofAmerica,3DivisionofInfectiousDiseaseandInternationalHealth,Centerfor Global Health, University of Virginia, Charlottesville, Virginia, United States of America, 4Medical Informatics and Systems Division, Virginia Bioinformatics Institute, VirginiaTech,Blacksburg,Virginia,UnitedStatesofAmerica,5DepartmentofBiologicalSciences,VirginiaTech,Blacksburg,Virginia,UnitedStatesofAmerica Abstract Clostridium difficile is an anaerobic bacterium that has re-emerged as a facultative pathogen and can cause nosocomial diarrhea,colitisorevendeath.Peroxisomeproliferator-activatedreceptor(PPAR)chasbeenimplicatedinthepreventionof inflammationinautoimmuneandinfectiousdiseases;however,itsroleintheimmunoregulatorymechanismsmodulating host responses to C. difficile and its toxins remains largely unknown. To characterize the role of PPARc in C. difficile- associateddisease(CDAD),immunityandgutpathology,weusedamousemodelofC.difficileinfectioninwild-typeandT cell-specific PPARc null mice. The loss of PPARc in T cells increased disease activity and colonic inflammatory lesions following C. difficile infection. Colonic expression of IL-17 was upregulated and IL-10 downregulated in colons of T cell- specificPPARcnullmice.Also,boththelossofPPARcinTcellsandC.difficileinfectionfavoredTh17responsesinspleen andcoloniclaminapropriaofmicewithCDAD.MicroRNA(miRNA)-sequencinganalysisandRT-PCRvalidationindicatedthat miR-146bwassignificantlyoverexpres