Activation of the host cell proinflammatory interleukin-8 response by Chlamydia trachomatis
Activation of the host cell proinflammatory interleukin-8 response by Chlamydia trachomatis
复制标题
DOI：
10.1111/j.1462-5822.2006.00747.x
复制
发表时间：
2006-11-01
影响因子：
3.4
通讯作者：
Stephens, Richard S.
中科院分区：
文献类型：
--
作者：
Buchholz, Kerry R.;Stephens, Richard S.
衣原体相关疾病是由反复或慢性感染后的炎症相关组织损伤引起的；然而，诱导炎症反应的机制尚不清楚。炎性细胞因子白介素-8 （IL-8）是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的。我们假设IL-8是通过激活衣原体感染细胞内的宿主信号通路而诱导的。IL-8的诱导需要感染后15小时细菌蛋白的合成，因此，IL-8 mRNA的增加是由于衣原体生长或15hpi时产生的细菌产物。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启动子和宿主NF κ B信号通路的AP-1、NFIL6 （C/EBP β）和NF κ B转录调控位点是沙眼衣原体诱导IL-8所必需的。我们得出结论，沙眼衣原体在发育中期产生的生长依赖因子通过激活宿主信号通路诱导其感染的上皮细胞内的IL-8。
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/EBP beta) and NF kappa B transcriptional regulatory sites of the IL-8 promoter and the host NF kappa B 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.