沙眼衣原体感染诱生的活性氧(ROS)对宿主细胞坏死的影响

 目的 初步观察沙眼衣原体(Chlamydia trachomatis)感染诱生的活性氧(reactive oxygen species,ROS)对宿主细胞坏死的影响,为沙眼衣原体与宿主细胞死亡机制的相互作用提供初步线索。 方法 沙眼衣原体小鼠生物型(Chlamydia muridarum)感染L929细胞,分别在12 h、24 h收集细胞,检测其ROS、坏死率及16srRNA表达,并检测应用ROS抑制剂(diphenyliodonium chloride,DPI)后上述指标及caspase 1的活性情况。结果 沙眼衣原体感染了L929细胞。与对照组相比,实验组在12 h、24 h 2个检测时间点的ROS、细胞坏死率及16srRNA表达均有显著增加,且随时间延长增加趋势加大(P＜0.05)。用药物DPI处理感染的L929细胞后,实验组与对照组相比不但ROS水平降低,而且伴随着细胞坏死率、caspase 1活性和16srRNA表达的降低(P＜0.05)。结论 沙眼衣原体感染L929细胞后诱生的ROS一定程度上促进了宿主细胞的坏死。

Reactive oxygen species (ROS) mediated necrosis of host cells induced by Chlamydia trachomatis infection

Objective To explore the influence of reactive oxygen species (ROS) to necrosis of host cells induced by Chlamydia trachomatis infection, so as to provide clues for the interaction of C. trachomatis infection and the death mechanism of host cell. Methods L929 cells were infected by C. muridarum, and were collected at 12 and 24 hours post infection. The levels of ROS, necrosis and 16srRNA production were detected. After diphenyliodonium chloride (DPI), a ROS inhibitor, was used to treat the infected cells, the levels of ROS, necrosis, 16srRNA production and caspase 1 activity were detected. Results The levels of ROS, necrosis and 16srRNA production in C. trachomatis infected L929 cells at 12 and 24 hours post infection were significantly higher than those of uninfected control group(P＜0.05). When ROS production was inhibited by DPI treatment, the cell necrosis rate, caspase 1 activity and 16srRNA production were coincidently reduced compared with DPI untreated control(P＜0.05). Conclusions ROS induced by C. trachomatis infected L929 cells promotes the necrosis of the host cells.