Primary Study On The Role Of STAT3-TLR2Signaling Axis In Chlamydia Trachomatis Persistent Infection

Objective:Chlamydia trachomatis (Ct) is prevalent sexually transmitted bacterial pathogen, and inflammation is the main pathological characteristics of its infection. In state of chlamydia trachomatis persistent infection, the STAT3-TLR2axis may be activated mediating abnormal secretion of inflammatory cytokines. Therefore, in order to explore the mechanism of abnormal inflammatory cytokine secretion, and to provide theoretical and experimental basis for the prevention and treatment of chlamydial infection, the role of STAT3-TLR2axis in Ct infected cells was studied.Method:We established the mock infection, acute infection and IFN-y induced persistent infection model of Ct in HeLa cell. RNAi technology to down-regulate the expression of STAT3in HeLa was adapted. Gene transcription, cytokine secretion and protein expression were detected by using qRT-PCR, ELISA and WB respectively in STAT3-TLR2signaling axis in each Ct infection model.Results:Persistent Ct infections upregulated the transcription of TLR2, IL-6and STAT3, significantly increased both the secretion of cytokine IL-6and the expression of STAT3and TLR2, moreover, enhanced the activation of STAT3simultaneously. The expression of IL-6and TLR2is closely associated with the expression of STAT3. After downregulating the expression of STAT3gene in HeLa cell, persistent Ct infectious HeLa cell secretion of IL-6and IL-1α level and protein expression of TLR2level were significantly lower, and the secretion of IL-6and IL-la was significantly related to the interference effect of STAT3expression.Conclusion:1. In the Ct persistent infection induced by IFN-y, the secretion of inflammatory cytokines IL-6, IL-1α and the expression of STAT3, TLR2increased significantly in HeLa cell.2. In the Ct persistent infection, the increase of IL-6, STAT3and TLR2showed higher correlation, and STAT3is a critical molecule in the secretion of inflammatory cytokines.3. In the process of Ct persistent infection, there are obvious activation of STAT3-TLR2signaling pathways.