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作者：苏真，邓威威，湛舒婷，梁盼盼，李美容，尹颂超，陈剑

通信作者：陈剑，E-mail:chenj8

作者单位：医院皮肤科，广东广州

苏真,邓威威,湛舒婷,等.红色毛癣菌、石膏样小孢子菌对人角质形成细胞TLR2/c-Jun、NF-κB信号通路的差异性诱导[J].皮肤性病诊疗学杂志，,28（1）：1-6.

基金项目：国家自然科学基金(编号：)

[摘要]目的:探讨不同生态学分类皮肤癣菌对人角质形成细胞TLR2/c-Jun、NF-κB信号通路的诱导。方法：将红色毛癣菌、石膏样小孢子菌分别与HaCaT细胞共培养24h后，蛋白免疫印迹检测p65、relb、IκB、c-Jun的总蛋白及其磷酸化水平。然后将红色毛癣菌、石膏样小孢子菌分别与HaCaT细胞TLR2敲除细胞株（HaCaTTLR2-/-细胞）共培养24h后，采用蛋白免疫印迹检测TLR2、c-Jun蛋白及其磷酸化水平。结果：HaCaT细胞感染红色毛癣菌后c-Jun蛋白磷酸化水平无明显变化，而感染石膏样小孢子菌后c-Jun蛋白磷酸化水平升高。p65、relb、IκB的总蛋白及其磷酸化水平在两种菌的感染下均无明显变化。HaCaTTLR2-/-细胞感染红色毛癣菌后c-Jun蛋白磷酸化水平明显降低，而感染石膏样小孢子菌后c-Jun蛋白磷酸化水平无明显变化。结论：红色毛癣菌与石膏样小孢子菌都可以通过TLR2激活人角质形成细胞c-Jun信号通路，但并未激活NF-κB信号通路。此外，TLR2可能和其他受体共同介导了红色毛癣菌、石膏样小孢子菌对c-Jun信号通路的差异性诱导。

[关键词]角质形成细胞；红色毛癣菌；石膏样小孢子菌；TLR2；c-Jun信号通路

[中图分类号]R［文献标识码］ADOI:10./j.issn.-..01.

DifferentialinductionofTLR2/c-JunandNF-κBsignalingpathwayinhumankeratinocytesinfectedbyTrichophytonrubrumandMicrosporumgypseum

SUZhen，DENGWeiwei，ZHANShuting，LIANGPanpan，LIMeirong，YINSongchao，CHENJian

TheThirdAffiliatedHospitalofSunYat-senUniversity,Guangzhou,China

Correspondingauthor:CHENJian,E-mail:chenj8

SUZhenandDENGWeiweicontributedequallytothiswork.

[Abstract]Objective：ToexploretheactivationofTLR2/c-JunandNF-κBsignalingpathwayinhumankeratinocytesinfectedbydifferentecologicalclassificationsofdermatophytes.Methods:Totalandphosphorylatedp65,relb,IκB,andc-JuninHaCaTcellsweredetectedbyimmunoblottingfollowingco-culturewitheitherTrichophytonrubrum(T.rubrum)orMicrosporumgypseum(M.gypseum)for24h.ImmunoblottingwasusedtoassessexpressionlevelsofTLR2,c-Jun,andphosphorylatedc-Junafterco-cultureofTLR2deficientHaCaTcells(HaCaTTLR2-/-cells)withT.rubrumandM.gypseumfor24h.Results:Co-cultureofHaCaTcellswithM.gypseum,butnotT.rubrum,significantlyincreasedthelevelsofphosphorylatedc-Jun.However,neitherT.rubrumnorM.gypseuminducedsignificantchangesinthetotalandphosphorylatedp56,relb,andIκBinHaCaTcells.FollowingTLR2knockoutinHaCaTcells,thelevelofphosphorylatedc-JundecreasedsignificantlyinHaCaTTLR2-/-cellsco-culturedwithT.rubrum,butnotM.gypseum.Conclusions:T.rubrumandM.gypseumcanactivatec-JunsignalingpathwaythroughTLR2inkeratinocytes,withoutactivationofNF-κBsignalingpathway.TLR2,togetherwithotherreceptors,maydominatethedifferentialinductionofc-JunpathwayinkeratinocytesinfectedbyT.rubrumandM.gypseum.

[Keywords]keratinocytes;Trichophytonrubrum;Microsporumgypseum;TLR2;c-Junsignalingpathway

Dermatophytosis,affectingmillionsofpeople,remainsanunsolvedworldwidepublichealthproblem,andcostsmorethanmilliondollarsannuallyintreatment.ItisestimatedthatmorethaneightmilliondollarsarespentonthetreatmentofdermatomycosisinUniteStates[1].T.rubrum,accountingforabout80%ofglobaldermatophytes,isthemainpathogenofdermatophytosis[2-3],andcancausemildinflammation[4].M.gypseum,ageophilicstrain,isararecauseofhumanskininfectionandtendstoinduceacuteinflammatoryresponse[4].Thedifferencesininflammatoryresponsescausedbydifferentecologicaldermatophyteshavelongbeenrecognizedasthe