pORF5 plasmid protein of Chlamydia trachomatis induces MAPK-mediated pro-inflammatory cytokines via TLR2 activation in THP-1 cells  

作　　者：ZHOU Hui HUANG QiuLin LI ZhongYu WU YiMou XIE XiaoBing MA KangKang CAO WenJuan ZHOU Zhou LU ChunXue ZHONG GuangMing 

机构地区：[1]Pathogenic Biology Institute,University of South China [2]Department of Laboratory Medicine,the First Hospital of Hunan University of Chinese Medicine [3]Department of General Surgery,the First Affiliated Hospital of University of South China [4]Department of Microbiology and Immunology,University of Texas Health Science Center,San Antonio,TX 78229,USA

出　　处：《Science China(Life Sciences)》2013年第5期460-466,共7页中国科学（生命科学英文版）

基　　金：supported by the National Natural Science Foundation of China(30970165,81102230);Team Project for the Technology Innovation of Higher Education of Hunan Province,China,2010

摘　　要：Infection with Chlamydia trachomatis induces inflammatory pathologies in the urogenital tract that can lead to infertility and ectopic pregnancy. Pathogenesis of infection has been mostly attributed to excessive cytokine production. However, precise mechanisms on how C. trachomatis triggers this production, and which protein（s） stimulate inflammatory cytokines remains unknown. In the present study, the C. trachomatis pORF5 protein induced tumor necrosis factor alpha （TNF-a）, interleukin-1 beta （IL-1β） and interleukin-8 （IL-8） in dose and time-dependent manners in the THP-1 human monocyte cell line. We found that intracellular p38/mitogen-activated protein kinase （MAPK） and extracellular signal-regulated kinase （ERK）/MAPK signaling pathways were required for the induction of TNF- a, IL-1β and IL-8. Blockade of toll-like receptor 2 （TLR2） signaling reduced induction levels of TNF-a, IL-8 and IL-1β. We concluded that the C. trachomatis pORF5 protein might contribute to the inflammatory processes associated with chlamydial infections.Infection with Chlamydia trachomatis induces inflammatory pathologies in the urogenital tract that can lead to infertility and ectopic pregnancy.Pathogenesis of infection has been mostly attributed to excessive cytokine production.However,precise mechanisms on how C.trachomatis triggers this production,and which protein(s) stimulate inflammatory cytokines remains unknown.In the present study,the C.trachomatis pORF5 protein induced tumor necrosis factor alpha(TNF-α),interleukin-1 beta(IL-1β) and interleukin-8(IL-8) in dose-and time-dependent manners in the THP-1 human monocyte cell line.We found that intracellular p38/mitogen-activated protein kinase(MAPK) and extracellular signal-regulated kinase(ERK)/MAPK signaling pathways were required for the induction of TNF-α,IL-1β and IL-8.Blockade of toll-like receptor 2(TLR2) signaling reduced induction levels of TNF-α,IL-8 and IL-1β.We concluded that the C.trachomatis pORF5 protein might contribute to the inflammatory processes associated with chlamydial infections.

关 键 词：Chlamydia trachomatis pORF5 plasmid protein mitogen-activated protein kinase proinflammatory cytokines TLR2 

分 类 号：R711.3[医药卫生—妇产科学]