INDUCTION OF ULCERATION AND SEVERE GASTRITIS IN MONGOLIAN GERBIL BY HELICOBACTER-PYLORI INFECTION

Specific pathogen-free Mongolian gerbils were infected orally with Hel icobacter pylori to establish a new small animal model of severe gastr itis H. pylori was recovered by culture from both antrum and body over a 16-week period after a single inoculation. The number of H. pylori colonising the antrum was about 100-fold higher than in the body, and this was consistent throughout the experiment. Histological examinatio n showed that all animals developed severe inflammation with infiltrat ion of polymorphonuclear leucocytes and mononuclear cells into the lam ina propria and submucosa of the antrum from 4 weeks after infection. From 8 weeks after infection, multifocal lymphoid follicles appeared i n the lamina propria and submucosa, and micro-erosions were also obser ved in the epithelial layer. At 16 weeks after infection, ulceration w ith disruption of the lamina muscularis mucosae was observed in the an tral mucosa. To determine whether H. pylori caused gastritis or not, i nfected gerbils were treated with amoxycillin. After the treatment, ga stritis could not be seen in the gastric mucosa. Therefore, the Mongol ian gerbil is a useful small animal model to study the pathogenesis of H. pylori in gastric ulceration and severe gastritis and to assess an ti-H. pylori treatment.