PATHOLOGICAL-CHANGES IN THE FORMATION OF HELICOBACTER PYLORI-INDUCED GASTRIC-LESIONS IN MONGOLIAN GERBILS

Citation
S. Takahashi et al., PATHOLOGICAL-CHANGES IN THE FORMATION OF HELICOBACTER PYLORI-INDUCED GASTRIC-LESIONS IN MONGOLIAN GERBILS, Digestive diseases and sciences, 43(4), 1998, pp. 754-765
Citations number
46
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
01632116
Volume
43
Issue
4
Year of publication
1998
Pages
754 - 765
Database
ISI
SICI code
0163-2116(1998)43:4<754:PITFOH>2.0.ZU;2-U
Abstract
We examined pathological changes in the formation of Helicobacter pylo ri-induced gastric lesions in Mongorian gerbils. H. pylori (NCTC11637) was orally administered once to the animals and was detected in the g astric mucosa of all gerbils given the bacteria. The number of viable H. pylori increased during the initial two weeks and thereafter reache d a plateau level. The initial pathological changes were found at one week, ie, edema/congestion and a white viscous substance only in the a ntrum. At two weeks, superficial damage appeared in the antrum, althou gh inflammatory cell infiltration had not occurred. Gastritis with lym phoid follicles was observed in the antrum and fundus from three weeks . At four weeks, mucosal lesions were detected as a few hemorrhagic sp ots in the fundus adjacent to the antrum. In the control animals, howe ver, no pathological changes were observed even at four weeks. In the gastric mucosa infected with H. pylori, myeloperoxidase activity was n egligible at two weeks, but was extremely elevated at four weeks. Simi larly, neutrophil chemotactic activity was only slightly increased at two weeks, but was markedly elevated at four weeks. These results indi cate that H. pylori infection induces initial pathological changes onl y in the antrum, but mucosal lesions occur in the fundus adjacent to t he antrum. Furthermore, it is demonstrated that the initial superficia l damage is generated by factors other than chemokines and neutrophil- associated factors, although mucosal inflammation may contribute to th e subsequent formation of lesions and ulcers.