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- 0、cagA- cagE+、cagA- cagE- 的幽门螺杆菌与中国人胃上皮细胞MGC 80 3共培养 ,分泌的IL 8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
Objective To study the effect of different cag pathogenicity island in clinical isolated Helicobacter pylori (H. pylori ) and various kinase inhibitors on H. pylori induced interleukin 8 (IL 8) secretion by gastric epithelial cells. Methods Gastric epithelial cells (MGC 803) were cocultured with clinical cagA + cagE +, cagA + cagE -, cagA - cagE +, cagA - cagE - H. pylori in vitro , respectively. By the end of culture, IL 8 protein secretion was assayed by ELISA. The effects 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 by gastric epithelial cells stemed from H. pylori stimulation were examined. Results cagA + cagE + H. pylori induced more IL 8 protein secretion than cagA + cagE - or cagA - cagE + H. pylori , but cagA - cagE - H. pylori didn′t induce IL 8 protein secretion. Further studies with gastric epithelial cells showed that IL 8 protein secretion induced by cagA + cagE + H. pylori was blocked by the PTK inhibitor herbimycin A but not by PKA inhibitor H7, PKC inhibitor calphostin C, and nor by PKG inhibitor KT5823. Conclusion The cagA + cagE + H. pylori significantly increases IL 8 secretion and this increase is dependent on PTK activation in gastric epithelial cell. [
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
2001年第6期672-675,共4页
Chinese Journal of Microbiology and Immunology
基金
广东省科委自然科学基金 ( 970 46 )
广东省医学科学基金 (B2 0 0 0 0 2 7)资助项目
