Pertussis Toxin Stimulates IL-17 Production in Response to Bordetella pertussis Infection in Mice 英文参考文献.docVIP

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Pertussis Toxin Stimulates IL-17 Production in Response to Bordetella pertussis Infection in Mice 英文参考文献.doc

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Pertussis Toxin Stimulates IL-17 Production in Response to Bordetella pertussis Infection in Mice 英文参考文献

PertussisToxinStimulatesIL-17ProductioninResponse toBordetellapertussisInfectioninMice CharlotteAndreasen¤,DanielA.Powell,NicholasH.Carbonetti* DepartmentofMicrobiologyandImmunology,UniversityofMarylandSchoolofMedicine,Baltimore,Maryland,UnitedStatesofAmerica Abstract InamousemodelofrespiratorytractinfectionbyBordetellapertussis,bacteriamultiplyintheairwaysoverthefirstweek andarethenclearedoverthenext3–4weeksbythehostimmuneresponse.Pertussistoxin(PT),avirulencefactorsecreted exclusively by B. pertussis, promotes bacterial growth in the airways by suppression and modulation of host immune responses.BycomparisonofwildtypeandPT-deficientstrains,weexaminedtheroleofPTinmodulatingairwaycytokine andchemokineresponsesaffectingneutrophilrecruitmentduringB.pertussisinfectioninmice.Wefoundthat,despiteearly inhibition of neutrophil recruitment by PT, high numbers of neutrophils were recruited to the airways by 4days post- infection with the wild type strain, but not with the PT-deficient strain, and that this correlated with upregulation of neutrophil-attracting chemokine gene expression. In addition, there was similar upregulation of genes expressing the cytokinesIL-17A(IL-17),TNF-aandIFN-c,indicatingamixedTh1/Th17response.ExpressionofIL-6,acytokineinvolvedin Th17induction,wasupregulatedearlierthantheIL-17response.WeshowedthatPT,ratherthanbacterialnumbers,was important for induction of these responses. Flow cytometric analysis revealed that the IL-17-producing cells were macrophagesandneutrophilsaswellasTcells,andwerepresentpredominantlyintheairwaysratherthanthelungtissue. Antibody neutralization of IL-17 significantly reduced chemokine gene expression and neutrophil recruitment to the airways,butonlymodestlyincreasedpeakbacterialloads.ThesedataindicatethatPTstimulatesinflammatoryresponsesby inductionofTh1-andTh17-associatedcytokines,includingIL-17,duringB.pertussisinfectioninmice,butaroleforIL-17in protectionagainsttheinfectionremainstobeestablished. Citation:AndreasenC,Pow