B cells promote obesity‐associated periodontitis and oral pathogen‐associated inflammation

Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society

关键词: B lymphocyte;    type 2 diabetes;    mouse model;    Porphyromonas gingivalis ;    cytokine;   

DOI  :  10.1189/jlb.4A0214-095R

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

IndividualswithT2DandPDsuffersignificantlyfromtheabilityofonediseasetointensifytheother.Disease‐associatedinflammationisonemechanismthoughttofuelthispathogenicfeed‐forwardloop.SeverallinesofevidenceindicatethatproinflammatoryBcellspromoteT2DandPD;thus,BcellsaretopcandidatesforacelltypethatpredisposesPDinT2D.TotestdirectlytheroleofBcellsinT2D‐associatedPD,wecomparedoutcomesfromoralPorphyromonasgingivalischallengeofleanWTorBcell‐nullmicewithoutcomesfrommicethatwereobeseandinsulin‐resistantbeforechallenge.ObeseWTmicerespondedtooralP.gingivalischallengewithsignificantperiodontalboneloss,whereasobeseBcell‐nullmicewereprotectedcompletelyfromPD.Bycontrast,leanWTandBcell‐nullmicesuffersimilarperiodontalbonelossinresponsetooralpathogen.Bcellsfromobese/insulin‐resistanthostsalsosupportoralosteoclastogenesisandbothoralandsystemicproductionofinflammatorycytokines,includingpro‐osteoclastogenicTNF‐αandMIP‐2,anorthologofhumanIL‐8.BcellsfurthermoreimpactATinflammationinobese,P.gingivalis‐infectedhosts.Takentogether,thesedatashowthatfundamentallydifferentmechanismsregulatePDinleanandobesehosts,withBcellsabletopromotePDonlyifthehostsare“primed”byobesity.Theseresultsjustifymoreintenseanalysisofobesity‐associatedchangesinBcellsthatpredisposePDinhumanT2D...

【 授权许可】

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