Background : H. pylori infection is associated with increased apoptosis of gastric epithelium. However, the mechanism remains unclear what product of the H. pylori causes apoptosis. This study was to investigate the roles of CagA, VacA protein and ammonia produced by H. pylori in inducing the apoptosis of gastric epithelium. Methods : Endoscopic biopsy samples were taken for rapid urease test, histology, and culture in 34 patients with peptic ulcer disease. And we analysed the ammonia level of gastric juice and CagA and VacA protein in serum. Apoptosis in situ was examined by using the methods of terminal uridine deoxynucleotidyl nick end-labelling (TUNEL). All patients infected by H. pylori were treated with antibiotics, and reevaluated the above studies after treatment. Results : A total of 34 patients with peptic ulcer disease were enrolled: 10 were uninfected and 24 patients were infected with H. pylori. Of the 24 infected patients, 11 harbored CagA+VacA+ strains and 10 were infected with CagA+VacA- strains. Three patients were infected with CagA-VacA- strains. The ammonia level of gastric juice in infected patients by H. pylori was significantly higher than that in uninfected and posteradication therapy (92.3±52.3 mM vs. 13.8±6.1 mM and 16.8±11.8 mM). Apoptosis indices in infected patients by H. pylori were higher than those in uninfected and posteradication therapy (12.3±3.4 vs. 7.6±2.2 and 8.2±3.8). The difference in apoptotic indices between the patients haboring CagA+VacA+strains (n=11) and CagA+VacA- strains (n=10) was not statistically significant (12.6±3.4 vs. 12.3±3.1). There was a positive correlation between apoptotic indices and ammonia concentration in the gastric juice (r=0.376, p<0.05). Conclusion : These results indicate that H. pylori infection and increased production of ammonia in gastric juice may induce gastric epithelial apoptosis.(Korean J Med 59:151-160, 2000)