TcpC secreting uropathogenic E.coli promoted kidney cells to secrete MIP-2 via p38 MAPK pathway
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- 英文论文题名：TcpC secreting uropathogenic E.coli promoted kidney cells to secrete MIP-2 via p38 MAPK pathway
- 论文作者：He Yujie ; Zhang Chong ; Fang Jie ; Yang Yingzhi ; Zhang Dayong ; Wang Baoming ; Wang Linyao ; Pan Jianping
- 英文论文作者：He Yujie ; Zhang Chong ; Fang Jie ; Yang Yingzhi ; Zhang Dayong ; Wang Baoming ; Wang Linyao ; Pan Jianping ; School of Medicine ; Zhejiang University City College
- 年：2016
- 作者机构：School of Medicine,Zhejiang University City College;
- 英文论文关键词：Uropathogenic E.coli ; Pyelonephritis ; TcpC ; MIP-2
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R692.7
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：1013k
- 原文格式：D
- 会议级别：全国
摘要
Background: Toll/interleukin-1 receptor domain containing protein encoded by E. coli(TcpC) is an important virulence factor in most strains of uropathogenic Escherichia coli(UPEC) and inhibits the macrophage-mediated innate immunity, which plays crucial role in the pathogenesis of pyelonephritis. Objectives: To examine the regulatory effects of TcpC on production of MIP-2 in kidney cells and its related mechanism. Methods: Mouse models with pyelonephritis were established by transurethral instillation of TcpC-secreting wild type UPEC CFT073(TcpCwt) or tcp C-knock out CFT073(TcpC-/-). HEK-293 cells were co-cultured with TcpCwt or TcpC-/- in transwell. MIP-2 concentrations were measured by ELISA. Signaling transduction proteins were analyzed by Western blot. Results: MIP-2 concentration in kidney homogenates from TcpCwt caused murine pyelonephritis models was significantly higher than that from TcpC-/- caused models. In vitro, TcpCwt dose-dependently promoted MIP-2 secretion by HEK-293 cells. Concentration of MIP-2 in culture supernatants of HEK-293 co-cultured with TcpCwt was profoundly higher than that co-cultured with TcpC-/-. In the presence of anti-TcpC antibody, this enhancement effect of TcpCwt on MIP-2 production was completely abrogated. TcpC-/- treatment had no effect on p38 MAPK pathway, while TcpCwt treatment resulted in the activation of p38 MAPK in HEK-293 cells. Inhibition of p38 MAPK could significantly decrease MIP-2 concentration and neutrophil recruitment activity in the supernatants of HEK-293 cells co-cultured with TcpCwt. Conclusion: TcpC could promote kidney cells to produce MIP-2 through p38 MAPK pathway, which might contribute to the characteristic histological change of pyelonephritis.
Background: Toll/interleukin-1 receptor domain containing protein encoded by E. coli(TcpC) is an important virulence factor in most strains of uropathogenic Escherichia coli(UPEC) and inhibits the macrophage-mediated innate immunity, which plays crucial role in the pathogenesis of pyelonephritis. Objectives: To examine the regulatory effects of TcpC on production of MIP-2 in kidney cells and its related mechanism. Methods: Mouse models with pyelonephritis were established by transurethral instillation of TcpC-secreting wild type UPEC CFT073(TcpCwt) or tcp C-knock out CFT073(TcpC~(-/-)). HEK-293 cells were co-cultured with TcpCwt or TcpC~(-/-) in transwell. MIP-2 concentrations were measured by ELISA. Signaling transduction proteins were analyzed by Western blot. Results: MIP-2 concentration in kidney homogenates from TcpCwt caused murine pyelonephritis models was significantly higher than that from TcpC~(-/-) caused models. In vitro, TcpCwt dose-dependently promoted MIP-2 secretion by HEK-293 cells. Concentration of MIP-2 in culture supernatants of HEK-293 co-cultured with TcpCwt was profoundly higher than that co-cultured with TcpC~(-/-). In the presence of anti-TcpC antibody, this enhancement effect of TcpCwt on MIP-2 production was completely abrogated. TcpC~(-/-) treatment had no effect on p38 MAPK pathway, while TcpCwt treatment resulted in the activation of p38 MAPK in HEK-293 cells. Inhibition of p38 MAPK could significantly decrease MIP-2 concentration and neutrophil recruitment activity in the supernatants of HEK-293 cells co-cultured with TcpCwt. Conclusion: TcpC could promote kidney cells to produce MIP-2 through p38 MAPK pathway, which might contribute to the characteristic histological change of pyelonephritis.
Background: Toll/interleukin-1 receptor domain containing protein encoded by E. coli(TcpC) is an important virulence factor in most strains of uropathogenic Escherichia coli(UPEC) and inhibits the macrophage-mediated innate immunity, which plays crucial role in the pathogenesis of pyelonephritis. Objectives: To examine the regulatory effects of TcpC on production of MIP-2 in kidney cells and its related mechanism. Methods: Mouse models with pyelonephritis were established by transurethral instillation of TcpC-secreting wild type UPEC CFT073(TcpCwt) or tcp C-knock out CFT073(TcpC~(-/-)). HEK-293 cells were co-cultured with TcpCwt or TcpC~(-/-) in transwell. MIP-2 concentrations were measured by ELISA. Signaling transduction proteins were analyzed by Western blot. Results: MIP-2 concentration in kidney homogenates from TcpCwt caused murine pyelonephritis models was significantly higher than that from TcpC~(-/-) caused models. In vitro, TcpCwt dose-dependently promoted MIP-2 secretion by HEK-293 cells. Concentration of MIP-2 in culture supernatants of HEK-293 co-cultured with TcpCwt was profoundly higher than that co-cultured with TcpC~(-/-). In the presence of anti-TcpC antibody, this enhancement effect of TcpCwt on MIP-2 production was completely abrogated. TcpC~(-/-) treatment had no effect on p38 MAPK pathway, while TcpCwt treatment resulted in the activation of p38 MAPK in HEK-293 cells. Inhibition of p38 MAPK could significantly decrease MIP-2 concentration and neutrophil recruitment activity in the supernatants of HEK-293 cells co-cultured with TcpCwt. Conclusion: TcpC could promote kidney cells to produce MIP-2 through p38 MAPK pathway, which might contribute to the characteristic histological change of pyelonephritis.
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