Gastritis induced by Helicobacter pylori in Mongolian gerbils with gastric ulcer

Abstract

Infection with Helicobacter pylori is principal cause of chronic gastritis and is involved in peptic ulcer diseases. Gastric ulcer often coexists with chronic gastritis in humans. Recently, it has been reported that infection with this organism causes gastritis in Mongolian gerbils. In this study, we examined whether existence of gastric ulcer affects the development of gastritis induced by H. pylori, in Mongolian gerbils. We also investigated the effect of H. pylori-infection on gastric ulcer healing. Male Mongolian gerbils weighing about 40 g and H. pylori ATCC 43504 were used in this study. In control animals, H. pylori (1 x 108 CFUs) was orally inoculated with a feeding needle. In the other animals, gastric ulcers were produced by application of acetic acid. A plastic tube 4 mm in diameter was held against the serosa of anterior wall of the stomach at the junction of the body and the antrum, and 60 pl of 100% acetic acid was poured into the tube. The Mongolian gerbils were divided into two groups 24 hr after the production of ulcer. The animals belonging to the first group were inoculated with H. pylori (1 X 10 s CFUs). In the second group, vehicles were administered orally. The Mongolian gerbils were killed on days 30 and 60 after the inoculation (n=6-9). For the histological examination, each stomach was fixed in 10% neutral buffered formalin, sectioned into 6-[am pieces, and stained with hematoxylin and eosin. For the identification of H. pylori, sections were stained by the immunoperoxidase method with rabbit anti-H, pylori antibody. In controls, approximately 70% of animals were infected with H. pylori. In Mongolian gerbils with gastric ulcer, all of six animals were infected by days 30 and 60. In controls, infection with H. pylori caused superficial erosion in the pyloric mucosa. Leukocyte infiltration and lymphoid follicles were seen mainly in submucosal layer. In Mongolian gerbils with ulcer those were infected with H. pylori, such inflammatory responses were observed mainly in the mucosal layer and inflammation was more severe than that in controls. These histological changes occurred even in the mucosa distant from ulcerous area~ On the other hand, in uninfected animals, inflammation appeared only in ulcerous area. On day 60, five of seven ulcers had healed in uninfected animals, whereas in the infected group, all of six animals had an ulcer. These results suggest that existence of gastric ulcer affects host response to H. pylori, resulting in severe gastritis and infection with H. pylori delays gastric ulcer healing.