cagA +cagE + Helicobacter pylori induced interleukin 8 secretion in gastric epithelial cells and its dependence on protein tyrosine kinase activation
- VernacularTitle:诱导胃上皮细胞白细胞介素-8分泌的幽门螺杆菌基因型
- Author:
Jieli WU
;
Xingxiang HE
;
Guobin WANG
- Publication Type:Journal Article
- Keywords:
Helicobacter pylori;
?Interleukin 8;
?Protein kinase
- From:
Chinese Journal of Laboratory Medicine
2001;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of different cag pathogenicity island in Helicobacter pylori ( Hp ) from Chinese patients and various kinase inhibitors on Hp 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 - Hp in vitro, respectively. At the end of culture, IL 8 protein secretion was assayed by ELISA. The effect of the inhibitor of protein kinase A(PKA), C, G, protein tyrosine kinase(PTK) was analyzed on IL 8 protein secretion in gastric epithelial cells by Hp stimulation. Results cagA +cagE + Hp induced IL 8 protein secretion higher than cagA + cagE - or cagA -cagE + Hp , but cagA -cagE - Hp didn′t increase IL 8 protein secretion in gastric epithelial cells. Further studies with gastric epithelial cell showed that IL 8 protein secretion induced by cagA +cagE + Hp was blocked by the PTK inhibitor herbimycin A but not by PKA inhibitor H7, PKC inhibitor calphostin C, and PKG inhibitor KT5823. Conclusion cagA +cagE + Hp significantly increases IL 8 protein secretion and it depends on PTK activation in gastric epithelial cells.
