Helicobacter pylori infection affects gastric ulcer healing in Japanese monkeys

Although peptic ulcer frequently recurs in the presence of Helicobacter pylori infection, the effects of H. pylori on ulcer healing have yet to be studied in detail. Using an animal model, we examined the effects of H. pylori infection on the healing of peptic ulcer in Japanese macaques. Forty-four Japanese macaques, aged 5 years, were randomly divided into two groups, an H. pylori-infected group and a control group, with 22 animals in each. A total of 10(9) colony forming units per ml of an H. pylori strain clinically isolated from patients positive for the cagA gene, the vacA gene, and vacuolizing toxin production, was inoculated into the stomachs of the monkeys to induce H. pylori-associated gastritis. The monkeys were examined by endoscopy, and then 0.1 ml of 10% ammonia solution was injected into the angulus to produce an active ulcer. Endoscopic observations was performed every week for 8 weeks. Acid-reducing drugs and other cytoprotective agents were not administered during the 8-week observation period. No difference in the healing of the ulcers was seen between the two groups from the first to the third week. However, a significant delay in healing was noted in the H. pylori-infected group from the fourth week on wards (P < 0.05). At the sixth week, the proportion of ulcers in the S2 stage (presence of a complete scar) was 0% in the H. pylori-infected group and 38% in the control group, again indicating that healing was significantly delayed in the H. pylori-infected group (P = 0.0187). By the eighth week, the proportion of ulcers in S2 stage had increased to 18% in the H. pylori-infected group and 67% in the control group (P = 0.0719). In Japanese macaques with persistent H. pylori infection in the stomach, the speed of repair of the ulcer surface was reduced, leading to delayed ulcer healing, compared with the controls.