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
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.