Dynamic Innate Immune Responses of Human Bronchial Epithelial Cells to Severe Acute Respiratory Syndrome-Associated Coronavirus Infection 英文参考文献.docVIP

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Dynamic Innate Immune Responses of Human Bronchial Epithelial Cells to Severe Acute Respiratory Syndrome-Associated Coronavirus Infection 英文参考文献.doc

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Dynamic Innate Immune Responses of Human Bronchial Epithelial Cells to Severe Acute Respiratory Syndrome-Associated Coronavirus Infection 英文参考文献

DynamicInnateImmuneResponsesofHumanBronchial EpithelialCellstoSevereAcuteRespiratorySyndrome- AssociatedCoronavirusInfection TomokiYoshikawa1,TerenceE.Hill1,NaokoYoshikawa1,VsevolodL.Popov2,3,CristiL.Galindo4, HaroldR.Garner4,C.J.Peters1,2,3,Chien-Te(Kent)Tseng1,3 * 1DepartmentofMicrobiologyandImmunology,UniversityofTexasMedicalBranch,Galveston,Texas,UnitedStatesofAmerica,2DepartmentofPathology,UniversityofTexas MedicalBranch,Galveston,Texas,UnitedStatesofAmerica,3CenterforBiodefenseandEmergingInfectiousDiseases,UniversityofTexasMedicalBranch,Galveston,Texas,United StatesofAmerica,4TheMcDermottCenterforHumanGrowthandDevelopment,UniversityofTexasSouthwesternMedicalCenter,Dallas,Texas,UnitedStatesofAmerica Abstract Human lung epithelial cells are likely among the first targets to encounter invading severe acute respiratory syndrome- associatedcoronavirus(SARS-CoV).NotonlycanthesecellssupportthegrowthofSARS-CoVinfection,buttheyarealso capable of secreting inflammatory cytokines to initiate and, eventually, aggravate host innate inflammatory responses, causing detrimental immune-mediated pathology within the lungs. Thus, a comprehensive evaluation of the complex epithelialsignalingtoSARS-CoViscrucialforpavingthewaytobetterunderstandSARSpathogenesis.Basedonmicroarray- based functional genomics, we report here the global gene response of 2B4 cells, a cloned bronchial epithelial cell line derivedfromCalu-3cells.Specifically,wefoundatemporalandspatialactivationofnuclearfactor(NF)kB,activatorprotein (AP)-1,andinterferonregulatoryfactor(IRF)-3/7ininfected2B4cellsat12-,24-,and48-hrspostinfection(p.i.),resultingin theactivationofmanyantiviralgenes,includinginterferon(IFN)-b,-ls,inflammatorymediators,andmanyIFN-stimulated genes(ISGs).Wealsoshowed,forthefirsttime,thatIFN-bandIFN-lswerecapableofexertingpreviouslyunrecognized, non-redundant, and complementary abilities to limit SARS-CoV replication, even though their expression could not be detectedininfected2B4bronchialepithelia