cag致病岛的差异及不同激酶抑制剂对幽门螺杆菌诱导胃上皮细胞IL-8分泌的影响  

The effect of different cag pathogenicity island and various kinase inhibitors on Helicobacter pylori induced interleukin-8 secretion in gastric epithelial cells.

作　　者：何兴样[1] 胡品津[1] 何瑶[1] Jianfeng Li Jiangshe Fan 吴捷莉[4] 

机构地区：[1]中山医科大学附属第一医院消化内科,广州510080 [2]Department of Medicine [3]Department of Pathology [4]第一军医大学分校生物化学教研室,广州510315

出　　处：《现代消化及介入诊疗》2000年第4期23-27,共5页Modern Interventional Diagnosis and Treatment in Gastroenterology

基　　金：广东省科委自然科学基金资助(No.97046)

摘　　要：目的:分析中国临床分离的幽门螺杆菌的 cag 致病岛的差异和不同激酶抑制剂对幽门螺杆菌诱导中国人胃上皮细胞 IL-8分泌的影响。方法:在体外分别用中国临床分离的 cagA^+cagE^+、cagA^+cagE^-、cagA^-cagE^+、cagA^-cagE^-的幽门螺杆菌与中国人胃上皮细胞 MGC-803共培养,IL-8分泌用 ELISA 进行检测,比较蛋白激酶 A、C、G 和蛋白酪氨酸激酶的抑制剂对幽门螺杆菌诱导胃上皮细胞 IL-8分泌的影响。结果:cagA^+cagE^+幽门螺杆菌显著增加了胃上皮细胞 IL-8的分泌,cagA^+cagE^-、cagA^-cagE^+幽门螺杆菌作用次之,而 cagA^-cagE^-幽门螺杆菌不能增加胃上皮细胞 IL-8的分泌。蛋白激酶 A、C、G 的抑制剂不能阻断幽门螺杆菌增加胃上皮细胞 IL-8的分泌,而蛋白酪氨酸激酶的抑制剂阻断了幽门螺杆菌增加胃上皮细胞 IL-8的分泌。结论:cagA^+cagE^+幽门螺杆菌显著增加了胃上皮细胞 IL-8的分泌并且依赖于蛋白酪氨酸激酶的活性。To study the effect of cag pathogenicity island's difference in Chinese clinical isolated Helicobacter pylori(H.pylori)and various kinase inhibitors on H.pylori induced interleukin-8(IL-8) secretion in Chinese gastric epithelial cells.Method Chinese gastric epithelial cells(MGC-803)were cocultured with Chinese clinical cagA^+cagE^+,cagA^+cagE^-,cagA^-cagE^+,cagA^-cage^-H.pylori in vitro,respectively. At the end of culture,IL-8 protein secretion was assayed by ELISA.It was analyzed that the effect of the inhibitor of protein kinase A(PKA),protein kinase C(PKC),protein kinase G(PKG),protein tyrosine kinase(PTK)on IL- 8 protein secretion in gastric epithelial cells by H.pylori stimulation.Results:cagA^+cagE^+H.pylori induced IL-8 protein secretion higher than cagA^+cagE^-or cagA^-cagE H.pylori,but cagA^-cagE^-H.pylori didn't induce IL-8 protein secretion in gastric epithelial cells.Further studies with gastric epithelial cell showed that IL-8 protein secretion induced by cagA^+cagE^+H.pylori was blocked by the PTK inhibitor herbimycin A but not by the PKA inhibitor H7,PKC inhibitor calphostin C,and PKG inhibitor KT5823.Conclusion:The cagA^+cagE^+H.pylori significantly increases IL-8 Protein secretion and it depends on PTK activation in gastric epithelial cell.

关 键 词：CAG致病岛 激酶抑制剂 幽门螺杆菌 胃上皮细胞 IL-8 白细胞介素-8 蛋白激酶 Hp 基因亚型 

分 类 号：R392.12[医药卫生—免疫学]