ERK介导幽门螺杆菌HSP60感染胃上皮细胞的IL-8分泌  

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

作　　者：赵莹[1] 魏晓晴[1] 吕广艳[1] 高颖[1,2] 金海威[3] 

机构地区：[1]辽宁省医学细胞分子生物学重点实验室,辽宁大连116044 [2]大连医科大学生化教研室,辽宁大连116044 [3]大连医科大学口腔医学院基础教研室,辽宁大连116044

出　　处：《现代生物医学进展》2009年第16期3053-3055,共3页Progress in Modern Biomedicine

基　　金：辽宁省教育厅2009年度高等学校科研项目计划资助项目(2009A195)

摘　　要：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细胞中磷酸化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细胞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细胞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。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.

关 键 词：H.pylori—HSP60 ERK 胃上皮细胞 

分 类 号：R378.2[医药卫生—病原生物学]