Pathological changes in the formation of Helicobacter pylori-induced gastric lesions in Mongolian gerbils.

We examined pathological changes in the formation of Helicobacter pylori-induced gastric lesions in Mongorian gerbils. H. pylori (NCTC11637) was orally administered once to the animals and was detected in the gastric mucosa of all gerbils given the bacteria. The number of viable H. pylori increased during the initial two weeks and thereafter reached a plateau level. The initial pathological changes were found at one week, ie, edema/congestion and a white viscous substance only in the antrum. At two weeks, superficial damage appeared in the antrum, although inflammatory cell infiltration had not occurred. Gastritis with lymphoid follicles was observed in the antrum and fundus from three weeks. At four weeks, mucosal lesions were detected as a few hemorrhagic spots in the fundus adjacent to the antrum. In the control animals, however, no pathological changes were observed even at four weeks. In the gastric mucosa infected with H. pylori, myeloperoxidase activity was negligible at two weeks, but was extremely elevated at four weeks. Similarly, neutrophil chemotactic activity was only slightly increased at two weeks, but was markedly elevated at four weeks. These results indicate that H. pylori infection induces initial pathological changes only in the antrum, but mucosal lesions occur in the fundus adjacent to the antrum. Furthermore, it is demonstrated that the initial superficial damage is generated by factors other than chemokines and neutrophil-associated factors, although mucosal inflammation may contribute to the subsequent formation of lesions and ulcers.