Aim To investigate the effects of Helicobacter pylori(Hp) infection and CagA gene on the gastric epithelial cell proliferation and apoptosis, and investigate the mechanisms of Hp increasing the risk of development of gastric cancer.Methods Endoscopic gastric mucosal biopsies were taken from 127 patients(chronic superficial gastritis,CSG; chronic atrophic gastritis,CAG; chronic atrophic gastritis with intestinal metaplasia,CAGIM; dysplasia,DYS; gastric cancer,GC) and 14 normal subjects(NS).The gastric antral epithelial cell proliferation was evaluated by ki-67 immunohistochemical technique, apoptosis cells in the gastric mucosa were quantitated after terminal deoxynucleotidyl transferase mediated dUTP nick end-labelling and Hp CagA gene was detected by polymerase chain reaction(PCR).Results Ki-67 labelling index(LI) and apoptosis index(AI) of Hp positive patients were significantly higher than that of Hp negative patients or normal controls( P <0.05 and P<0.01) .The LI and AI in Hp positive CSG patients were significantly higher than that in Hp negative CSG patients ( P<0.01); there was no significant difference between the patients with Hp infection and without Hp infection of the other four groups.Patients infected with CagA + Hp had significantly higher LI and much lower AI than that infected with CagA - Hp( P<0.05 ).The AI and LI had a positive correlation in Hp positive or negative CSG group and NS group, and a negative correlation in GC group.There was no correlation between LI or AI and the severity of gastritis.Conclusions Hp induced gastric epithelial proliferation and apoptosis predominantly in the early stage of Hp infection.CagA +Hp and CagA - Hp had different ability of inducing proliferation and apoptosis.Hp infection might lead to the imbalance of the AI/LI ratio and ultimately promote the development of gastric cancer.
