Helicobacter pylori-induced interleukin 8 secretion by gastric epithelial cells its relation to protein tyrosine kinase activation
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. [