摘要
Objective:Toidentifypresenceofinflammasomeactivatedinmousecochleawithsensorineuralhearingloss(SNHL)causedbycytomegalovirus(CMV)infection.Method:MCMVwasinjectedintotherightcerebralhemisphereinneonatalBALB/cmiceat2000pfuvirustiters.Auditorybrainstemresponses(ABRs)weretestedtoevaluatehearingat21days.HistopathologicalstudieswereconductedtoconfirmlocalizationsofMCMVinfectedcellsintheinnerear.Expressionofinflammasomerelatedfactorswasassessedbyimmunofluorescence,Quantitativereal-timePCRandWesternblotting.Results:InthemousemodelofCMVinducedSNHL,inflammasomerelatedkinaseCaspase-1anddownstreaminflammatoryfactorIL-1bandIL-18werefoundincreasedandactivatedafterCMVinfectioninthecochlea.Thesefactorscouldfurtherup-regulateexpressionofIL-6andTNFa.Theseinflammatoryfactorsareneurotoxicityandmaycontributetohearingimpairment.Furthermore,wealsodetectedsignificantlyincreasedAIM2proteinthataccumulatedintheSGNofcochleaewithCMVinfection.Significance:Wehaveshownthatinflammasomeasanovelinherentimmunitymechanismmaycontributetohearingimpairment.Conclusion:OurdataindicatethatimflammasomeassembleinmouseinnerearinresponsetoCMVinfection.WehaverevealedanovelpathologyeventinCMVinducedSNHLinvolvingactivationofinflammasomeinmousecochlea.Additionally,wehaveshownthatinflammasomemaybeanoveltargetforpreventionandtreatmentofCMVrelatedSNHL.
出版日期
2015年04月14日（中国期刊网平台首次上网日期，不代表论文的发表时间）
