ERK介导幽门螺杆菌HSP60感染胃上皮细胞的IL-8分泌

目的：探讨幽门螺杆菌热休克蛋白60（H．pylori—HSP60）感染胃上皮细胞后ERK与白介素-8（IL-8）分泌的关系。方法：利用ELISA技术，对活菌（IntactH．pylori）、死菌（Heat—killedH．pylori）及H．pylori—HSP60刺激胃上皮细胞KATOIII的IL_8蛋白分泌水平进行分析，观察IL-8随以上抗原浓度梯度的变化及ERK抑制剂PD98059对其分泌量的影响；利用Westernblot技术，观察KATOⅢ胞中磷酸化ERK随IntactH．pylori、Heat—killedH．pylori及H．pylori—HSP60刺激时间的变化状况。结果：IL-8的分泌随着IntactH．pylori、Heat—killedH．pylori及H．pylori—HSP60刺激浓度的升高而增高；H．pylori刺激KATOⅢ胞1h后ERK开始表达，其中IntactH．pylori在9h时表达达到高峰，Heat·killedH．pylori在24h时达到高峰，而H．pylori-HSP60刺激KATOⅢ胞6h后ERK开始表达，9h时达到高峰；PD98059抑制了H．pylori—HSP60诱导的IL-8的分泌。结论：ERK介导了H．pylori—HSP60感染的胃上皮细胞的IL-8的分泌。

Helicobacter pylori heat-shock protein 60 induces interleukin-8 via ERK pathway in human gastric epithelial cells

Objective： To investigate the relations of ERK and IL-8 secretion after H. pylori-HSP60 infection human gastric ep- ithelial （KATOⅢ） cells. Methods： KATOⅢ cells were co-cultured with several concentrations oflntact H. pylori, Heat-killed H. pylori, H. pylori-HSP60 and ERK inhibitor （PD98089）, and IL-8 secretion was measured by ELISA; After KATOⅢ cells were stimulated by Intact H. pylori, Heat-killed H. pylori or H. pylori-HSP60, the time-course ofp-ERK expression was observed by Western blot. Results： Intact H. pylori, Heat-killed H. pylori and H. pylori-HSP60 induced IL-8 production in a dose-dependent manner in KATOⅢ cells. P-ERK was activated by H. pylori at lh and peaked at 24h and 9h by Intact H. pylori and Heat-killed H. pylori, respectively. However, p-ERK activation was observed at 6h and peaked at 9h by H. pylori-HSP60 stimulation. P-ERK activation was significantly decreased by PD98059. Conclusion： H. pylori-HSP60 induces IL-8 via ERK pathway in human gastric epithelial cells.