Buchholz Kerry R, Stephens Richard S
Program in Infectious Diseases and Immunity, University of California, Berkeley, CA 94720, USA.
Cell Microbiol. 2006 Nov;8(11):1768-79. doi: 10.1111/j.1462-5822.2006.00747.x. Epub 2006 Jun 27.
Diseases associated with Chlamydia are caused by inflammation-associated tissue damage following repeated or chronic infection; however, the mechanism by which the inflammatory response is induced is unknown. The inflammatory cytokine interleukin-8 (IL-8) is produced by C. trachomatis-infected epithelial cells in a bacterial growth-dependent manner. We hypothesized that IL-8 is induced through activation of host signalling pathways within Chlamydia-infected cells. Bacterial protein synthesis occurring after 15 h post infection (hpi) was required for the induction of IL-8, thus, increases in IL-8 mRNA are due to chlamydial growth or a bacterial product produced at 15 hpi. The induction of IL-8 was not dependent on soluble factors in the supernatant of C. trachomatis-infected cells and therefore was associated with an internal cellular signal. The AP-1, NFIL6 (C/EBPbeta) and NFkappaB transcriptional regulatory sites of the IL-8 promoter and the host NFkappaB signalling pathway were necessary for IL-8 induction by C. trachomatis. We conclude that a C. trachomatis growth-dependent factor produced at mid-developmental stage induces IL-8 within the epithelial cell it infects through activation of host signalling pathways.
与衣原体相关的疾病是由反复或慢性感染后炎症相关的组织损伤引起的；然而，诱导炎症反应的机制尚不清楚。炎性细胞因子白细胞介素-8（IL-8）由沙眼衣原体感染的上皮细胞以细菌生长依赖的方式产生。我们假设IL-8是通过衣原体感染细胞内宿主信号通路的激活而诱导产生的。感染后15小时（hpi）后发生的细菌蛋白质合成是诱导IL-8所必需的，因此，IL-8 mRNA的增加是由于衣原体生长或在15 hpi时产生的细菌产物所致。IL-8的诱导不依赖于沙眼衣原体感染细胞上清液中的可溶性因子，因此与细胞内信号有关。IL-8启动子的AP-1、NFIL6（C/EBPβ）和NFκB转录调控位点以及宿主NFκB信号通路是沙眼衣原体诱导IL-8所必需的。我们得出结论，在发育中期产生的沙眼衣原体生长依赖性因子通过激活宿主信号通路在其感染的上皮细胞内诱导IL-8。
