美国国立卫生研究院资助项目.
This work was supported by a grant from National Institutes of Health(NIH).
沙眼衣原体感染可导致沙眼、性传播性疾病、不孕症等疾病,主要病理表现是炎症反应引起的组织损伤和瘢痕.因此,沙眼衣原体诱导产生的炎症因子是导致疾病的关键,沙眼衣原体可直接感染内皮细胞产生各种前炎因子,但其机制目前还不清楚.通过ELISA和免疫印迹等方法,检测到沙眼衣原体感染HeLa229细胞可产生IL-8,IL-1α,IL-1β,IL-6等前炎因子,并且沙眼衣原体感染可以主要激活宿主细胞MAPK/ERK和MAPK / P38信号通路. 抑制MAPK/ERK和MAPK / P38信号通路显示,两条通路在沙眼衣原体感染过程中参与调节不同的炎症因子产生.MAPK / P38信号通路的活化参与调控IL-1α,IL-6的产生,而IL-8则同时受MAPK/ERK 和 MAPK/P38 两条通路的调控.
Chlamydial infection in human urogenital tract induces inflammation and causes tissue damage and scarring. It is thought that cytokine production by the Chlamydia-infected cells plays a key role in chlamydial disease processes. Although many cytokines have been detected during chlamydial infection, little is known about the molecular mechanisms on how Chlamydia triggers and sustains the inflammatory cytokine cascades. In the current study, chlamydial infection of the human cervical epithelial cell line HeLa cells can induce the production of IL-8, IL-1α, IL-1β and IL-6. Using inhibitors for probing intracellular kinase signaling pathways required for the Chlamydia-induced cytokines, it was found that the Chlamydia-activated MAPK / P38 pathway is required for the chlamydial induction of IL-1α and IL-6 while both the Chlamydia-activated MAPK/ERK and MAPK/P38 pathways contribute to the production of IL-8.
程文,陈凡,余平,钟光明. MAPK/ERK 和 MAPK/P38 信号通路的活化参与沙眼衣原体诱导前炎因子的产生[J].生物化学与生物物理进展,2008,35(1):56-62
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