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1、IntensiveCareMedDOI10.1007/s00134-016-4544-8UNDERSTANDINGTHEDISEASEUnderstandinghost–pathogeninteractionK.Asehnoune1*,J.Villadangos2,3andR.S.Hotchkiss4©2016Springer-VerlagBerlinHeidelbergandESICMIntroductioninjuriesplayanimportantroleintheresponseofthehostAstrongresponsetopathogensismandatoryfo
2、rsur-againstthepathogen.These“dangersignals”arecalledvivalofthehost.However,thelocaldefencemechanismsdangerassociatedmolecularpatterns(DAMP)oralarm-maybedetrimentalwhenoverwhelmedand/orspreadins.Theendogenousproductsofinjuredcellsbecomesystemically.extracellularDAMPs(HMGB1,S100proteins,extracel
3、lu-larRNA,DNAandhistones)and,likePAMPissuedfromRecognitionof pathogensby thehostinducespathogens,theyactivatePRRaswellastheformationofinflammatoryresponsecellsurfacesignalosomes[4].ActivationofsignalosomesSpecificreceptorscalledpatternrecognitionreceptorsmediatestheonsetofapoptosis.Thisintrinsi
4、cprocessof(PRR)sensetheinterfacebetweenepitheliumandorgansremovingorrecyclingdamagedproteinsororganellesinawaythatrapidlyinducesastronginflammatorythatinduceapoptosisclearlyevokesautophagy.Whenresponsetokillthepathogens(Fig. 1)[1].PRRsrecog-autophagyisalteredanoverwhelmed,aninflamma-nizeconserv
5、edstructuresonpathogenscalledpathogen-toryresponsemayoccurinducingorgandysfunction.associatedmolecularpatterns(PAMPs).FiveclassesofInflammasomesmayalsomediatepyroptosis,aparticu-PRRincludingToll-likereceptors(TLRs),nucleotideoli-larformofprogrammedcelldeaththatreleasescellulargomerizationdomain
6、-likereceptors(NLRs),RIG-I-likedebrisextracellularly,therebyincreasingtheinflamma-receptors,C-typelectinreceptors,andabsenceinmela-toryprocess[5].Inconclusion,aninfectionmayinducenoma2(AIM2)-likereceptorshavebeendescribed[2].organdysfunctionthroughanexcessiveinflammatoryThesePRRssharecommonprop
7、ertiesexplainingtheirresponsebytwomechanisms:(1)directrecognitionofhighefficiency:(1)Expressiononepithelial,endothelial,thepathogenbythehost(interactionPAMP–PRR)and/innateandadaptiveimmunecells;(2)PRRactivationor(2)alterationofthe
