| Abstract: | Objective: To investigate pathological changes occurring in the stomach of the Mongolian gerbil during long‐term Helicobacter pylori infection. Methods: Four‐week‐old male Mongolian gerbils were used, which were free from specific pathogens. Eighty Mongolian gerbils were inoculated orally with a suspension of H. pylori NCTC 11637 (0.5 mL, 2 × 1010 CFU/L) in a Brucella broth. To act as controls, a further 30 gerbils were fed with a Brucella broth only. Infected gerbils were killed 10, 25, 45, 55 and 65 weeks after infection. Control gerbils were killed at 10, 45 and 65 weeks. The stomach of each gerbil was removed and opened. Stomach samples for histological examination were fixed in neutral buffered formalin, embedded in paraffin, sectioned and stained with hematoxylin and eosin for analyzing histological changes, Giemsa stain for detecting H. pylori and Alcian blue (AB)/periodic acid?Schiff stain for examining intestinal metaplasia. Results: The Mongolian gerbil model for studying long‐term H. pylori infection was successfully established. Helicobacter pylori induced a progression from normal gastric mucosa to chronic gastritis, glandular atrophy, intestinal metaplasia and dysplasia, although no adenocarcinomas were found in the experimental animals. Conclusions: Helicobacter pylori NCTC 11637 is able to easily colonize the glandular stomach mucosa of the Mongolian gerbil. This model is stable, and the histological changes observed in the stomach are similar to those that occur in humans with H. pylori infection. |
