Sidestream Smoke Exposure Increases the Susceptibility of Airway Epithelia to Adenoviral Infection 英文参考文献.docVIP

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Sidestream Smoke Exposure Increases the Susceptibility of Airway Epithelia to Adenoviral Infection 英文参考文献.doc

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SidestreamSmokeExposureIncreasestheSusceptibility ofAirwayEpitheliatoAdenoviralInfection PriyankaSharma1,AbimbolaO.Kolawole1,SusanB.Core2,AdrianaE.Kajon2*, KatherineJ.D.A.Excoffon1* 1Department of Biological Sciences, Wright State University, Dayton, Ohio, United States of America, 2Infectious Disease Program, Lovelace Respiratory Research Institute,Albuquerque,NewMexico,UnitedStatesofAmerica Abstract Background: Although significant epidemiological evidence indicates that cigarette smoke exposure increases the incidenceandseverityofviralinfection,themolecularmechanismsbehindtheincreasedsusceptibilityoftherespiratory tracttoviralpathogensareunclear.Adenovirusesarenon-envelopedDNAvirusesandimportantcausativeagentsofacute respiratorydisease.TheCoxsackievirusandadenovirusreceptor(CAR)istheprimaryreceptorformanyadenoviruses.We hypothesized that cigarette smoke exposure increases epithelial susceptibility to adenovirus infection by increasing the abundanceofapicalCAR. MethodologyandFindings:Culturedhumanairwayepithelialcells(CaLu-3)wereusedasamodeltoinvestigatetheeffect of sidestream cigarette smoke (SSS), mainstream cigarette smoke (MSS), or control air exposure on the susceptibility of polarized respiratory epithelia to adenoviral infection. Using a Cultex air-liquid interface exposure system, we have discovered novel differences in epithelial susceptibility between SSS and MSS exposures. SSS exposure upregulates an eight-exonisoformofCARandincreasesadenoviralentryfromtheapicalsurfacewhilstMSSexposureissimilartocontrol airexposure.Additionally,thelevelofcellularglycogensynthasekinase3b(GSK3b)isdownregulatedbySSSexposureand treatmentwithaspecificGSK3binhibitorrecapitulatestheeffectsofSSSexposureonCARexpressionandviralinfection. Conclusions:ThisisthefirsttimethatSSSexposurehasbeenshowntodirectlyenhancethesusceptibilityofapolarized epitheliumtoinfectionbyacommonrespiratoryviralpathogen.Thisworkprovidesanovelunderstandingoftheimpactof SSSontheburdenofrespiratoryviralinfe