Comparison of pathologic changes in Helicobacter pylori-infected Mongoliangerbils and humans

Helicobacter pylori has been recognized as a pathogen causing gastroduodena l disease, with adequate evidence to prove this relation in clinical resear ch. Available animal models, however, were inadequate until 1995, when a ne w animal model of H. pylori infection was established using Mongolian gerbi ls. In this study we compared pathological changes in seven H. pylori-infec ted Mongolian gerbils with ulcers to five patients with gastric ulcer who u nderwent operation. All of the animals showed positive reactions for both H . pylori culture and serum anti-II pylori antibody titer. All human subject s had H. pylori on the mucosal surface. Thus, inflammatory cell infiltratio n in the pyloric gland area was observed throughout almost all layers in th e animals. In contrast, inflammation was observed in the surface layer of t he mucosa in the pyloric gland area in the human subjects. Lymph follicle f ormation was observed more often in humans than in the animals. Inflammatio n of the fundic gland area in both groups was weaker than of the pyloric gl and area and was observed within the mucosa. Histological changes observed in both groups were chronic active gastritis, lymph follicles, and intestin al metaplasia in the stomach. H. pylori-associated gastritis in humans is c haracterized by erosion, inflammation with neutrophil infiltration, lymph f ollicles, intestinal metaplasia, and atrophy. These findings are similar to those in this animal model. Thus, H. pylori infection might participate in the pathogenesis of gastroduodenal mucosal damage. In conclusion, the Mong olian gerbil is a good animal model for H. pylori-associated gastric diseas es, and it might be useful for investigating the pathogenesis of H. pylori infection.