ESTABLISHMENT OF NEW SMALL ANIMAL-MODEL FOR HUMAN GASTRIC HELICOBACTER-PYLORI INFECTION

Objective. To develop a small animal model of Helicobacter pylori infection, and to clarify its pathogenicity and the role of the immune system in the infectious process. Design. In experimental work, the oral route of infection appears the most suitable at present. We therefore expected to successfully infect the gastric mucosa by administering a large amount of H. pylori orally. Method. We administered one oral dose of 2 ml (10(8) organisms/ml) of a broth culture of any of four isolates of human H. pylori to both BALB/C nude and BALB/C euthymic mice. We then investigated whether H. pylori had infected the stomach and duodenum of both mice strains. The stomach and duodenum of both nude and euthymic mice were examined histologically over a follow-up period of 20 weeks. Results. The gastric mucosa of nude mice was continuously (20 weeks) and that of thymic mice temporarily (2 weeks) colonized by orally administered fresh human isolates, with development of gastritis and gastric ulcer, but not by a laboratory-adapted strain. Following colonization, gastritis and duodenitis were produced and the presence of bacteria in gastric mucus was pathologically proven in all infected animals. Conclusion. We have established the first reported rodent model of H. pylori-associated gastritis, demonstrating that the organism is pathogenic and that the immune system plays a role in the infectious process. Conclusion. We have established the first reported rodent model of H. pylori-associated gastritis, demonstrating that the organism is pathogenic and that the immune system plays a role in the infectious process.