Mycobacterium tuberculosis Induces an Atypical Cell Death Mode to Escape from Infected Macrophages 英文参考文献.docVIP

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Mycobacterium tuberculosis Induces an Atypical Cell Death Mode to Escape from Infected Macrophages 英文参考文献.doc

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Mycobacterium tuberculosis Induces an Atypical Cell Death Mode to Escape from Infected Macrophages 英文参考文献

MycobacteriumtuberculosisInducesanAtypicalCell DeathModetoEscapefromInfectedMacrophages JinheeLee1,TeresaRepasy1,KadambaPapavinasasundaram2,ChristopherSassetti2,3,HardyKornfeld1* 1Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America, 2Department of Microbiology and PhysiologicalSystems,UniversityofMassachusettsMedicalSchool,Worcester,Massachusetts,UnitedStatesofAmerica,3HowardHughesMedicalInstitute,Universityof MassachusettsMedicalSchool,Worcester,Massachusetts,UnitedStatesofAmerica Abstract Background:MacrophagecelldeathfollowinginfectionwithMycobacteriumtuberculosisplaysacentralroleintuberculosis diseasepathogenesis.Certainattenuatedstrainsinduceextrinsicapoptosisofinfectedmacrophagesbutvirulentstrainsof M.tuberculosissuppressthishostresponse.WepreviouslyreportedthatvirulentM.tuberculosisinducescelldeathwhen bacillaryloadexceeds,20permacrophagebuttheprecisenatureofthisdemisehasnotbeendefined. Methodology/PrincipalFindings:Weanalyzedthecharacteristicsofcelldeathinprimarymurinemacrophageschallenged withvirulentorattenuatedM.tuberculosiscomplexstrains.Wereportthathighintracellularbacillaryburdencausesrapid and primarily necrotic death via lysosomal permeabilization, releasing hydrolases that promote Bax/Bak-independent mitochondrial damage and necrosis. Cell death was independent of cathepsins B or L and notable for ultrastructural evidence of damage to lipid bilayers throughout host cells with depletion of several host phospholipid species. These events require viable bacteria that can respond to intracellular cues via the PhoPR sensor kinase system but are independentoftheESX1system. Conclusions/Significance: Cell death caused by virulent M. tuberculosis is distinct from classical apoptosis, pyroptosis or pyronecrosis. Mycobacterial genes essential for cytotoxicity are regulated by the PhoPR two-component system. This atypical death mode provides a mechanism for viable bacilli to exit host macropha