Pathological Changes in the Formation of Helicobacter pylori-Induced Gastric Lesions in Mongolian Gerbils

We examined pathological changes in theformation of Helicobacter pylori-induced gastric lesionsin Mongorian gerbils. H. pylori (NCTC11637) was orallyadministered once to the animals and was detected in the gastric mucosa of all gerbils given thebacteria. The number of viable H. pylori increasedduring the initial two weeks and thereafter reached aplateau level. The initial pathological changes were found at one week, ie, edema/congestion and awhite viscous substance only in the antrum. At twoweeks, superficial damage appeared in the antrum,although inflammatory cell infiltration had notoccurred. Gastritis with lymphoid follicles was observedin the antrum and fundus from three weeks. At fourweeks, mucosal lesions were detected as a fewhemorrhagic spots in the fundus adjacent to the antrum.In the control animals, however, no pathologicalchanges were observed even at four weeks. In the gastricmucosa infected with H. pylori , myeloperoxidaseactivity was negligible at two weeks, but was extremely elevated at four weeks. Similarly, neutrophilchemotactic activity was only slightly increased at twoweeks, but was markedly elevated at four weeks. Theseresults indicate that H. pylori infection induces initial pathological changes only in theantrum, but mucosal lesions occur in the fundus adjacentto the antrum. Furthermore, it is demonstrated that theinitial superficial damage is generated by factors other than chemokines and neutrophil-associatedfactors, although mucosal inflammation may contribute tothe subsequent formation of lesions andulcers.