沙眼衣原体持续感染状态下STAT3-TLR2信号轴的变化初探  

Primary study on change of STAT3-TLR2 signaling axis in Chlamydia trachomatis persistent infection

作　　者：陈纯静[1] 陈恩[1] 林琳[1] 罗奇志[1] 李伟[1] 余平(指导)[1] 

机构地区：[1]中南大学基础医学院免疫学系,长沙410008

出　　处：《中国免疫学杂志》2015年第5期585-589,共5页Chinese Journal of Immunology

基　　金：国家自然科学基金项目(81371864);中南大学研究生自主探索创新基金项目(2014zzts295)资助

摘　　要：目的:探索在沙眼衣原体(Chlamydia trachomatis,Ct)持续感染状态下,STAT3-TLR2信号轴的变化,以及相关炎性细胞因子的异常分泌情况。方法:以He La细胞为研究对象,建立Ct的急性感染和IFN-γ诱导的持续性感染模型,采用qRT-PCR、Western blot、ELISA等方法比较不同感染状态下,He La细胞STAT3-TLR2信号轴相关分子如TLR2、STAT3及IL-1α等的变化。结果:在Ct持续性感染状态下,上皮细胞分泌的IL-1α以及STAT3和TLR2的表达均明显增加,且IL-1α的分泌、TLR2的表达与STAT3的蛋白表达和活化呈一致性的升高。结论:在IFN-γ诱导的Ct持续感染状态下,STAT3-TLR2信号轴相关分子存在明显活化。Objective：To explore in state of Chlamydia trachomatis persistent infection, the STAT3-TLR2 axis may be activated and mediating abnormal secretion of inflammatory cytokines. Methods： We established acute infection and IFN-γ induced persistent infection model of Ct in HeLa cell. Gene transcription, cytokine secretion and protein expression were detected by using qRT-PCR, ELISA and Western blot respectively in STAT3-TLR2 signaling axis in each Ct infection model. Results： Persistent Ct infections upregulated the transcription of TLR2,significantly increased both the secretion of inflammatory cytokine IL-1α and the expression of STAT3 and TLR2, moreover, enhanced the activation of STAT3 simultaneously. Conclusion： In the Ct persistent infection induced by IFN-γ,the STAT3-TLR2 signaling axis activated significantly in HeLa cell.

关 键 词：持续性感染 IFN-Γ 沙眼衣原体 STAT3 TLR2 IL-1Α 

分 类 号：R392[医药卫生—免疫学]