Gastric Ulcer, Atrophic Gastritis, and Intestinal Metaplasia Caused byHelicobacter pyloriInfection in Mongolian Gerbils

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Abstract
Helicobacter pylori infection is associated with gastroduodenal disease in humans. In this study we aimed to show this relationship directly in Mongolian gerbils. The animals were challenged orally with H. pylori and killed 1, 2, 3, and 6 months after inoculation for histologic and anti-H. pylori antibody titer examination. The spiral bacteria were observed in the mucus and gastric pits of all infected animals. A severe infiltration of the lamina propria by polymorphonuclear and mononuclear cells was seen 1 month after H. pylori inoculation. The submucosa was infiltrated by mainly mononuclear cells with formation of lymphoid follicles. Erosion of the gastric mucosa appeared soon after inoculation, whereas gastric ulcers, gastritis cystica profunda, and atrophy with goblet cell metaplasia occurred between 3 and 6 months after inoculation. In the duodenal mucosa a mild inflammatory cell infiltration with ballooning and diminished number of duodenal glands was seen. The IgG anti-H. pylori antibody titer increased gradually after 2 months of inoculation. Since the gastritis, gastric ulcers, atrophic gastritis, and intestinal metaplasia that developed in Mongolian gerbils were similar to those observed in humans, this model may be useful to study the therapy of gastric ulcer and, with a longer observation period, to confirm a possible relationship between H. pylori and malignancy.