gms | German Medical Science

Background: H. pylori infection in Mongolian gerbils is an established experimental model of gastric carcinogenesis which mimics H. pylori-positive patients developing gastric ulcer and gastric cancer, but effect of probiotic therapy on functional aspects of this infection remains unknown.

Methods: We compared the effects of intragastric (i.g.) inoculation of gerbils with H. pylori strain (cagA+ vacA+, 5x106 CFU/ml) with or without triple therapy including omeprazole, amoxicillin and tinidazol or probiotic bacteria Lacidofil. Histology of glandular mucosa, the viable H. pylori and density of H. pylori-colonization were evaluated. The gastric blood flow (GBF) was measured by H2-gas clearance method; the plasma gastrin and gastric luminal somatostatin were determined by RIA and expression of COX-2 and apoptotic Bax and Bcl-2 proteins were evaluated by Western Blot.

Results: The gastric H. pylori infection was detected in all animals by histology and H. pylori culture. Basal gastric acid was significantly reduced in H. pylori-infected animals but not in those with triple therapy or Lacidofil. Early lesions were seen already 4 weeks upon H. pylori-inoculation and consisted of chronic gastritis and glandular atypia associated with typical regenerative hyperplasia and increased mitotic activity and formation of apoptotic bodies. The H. pylori-infection was accompanied by the fall in GBF, the marked increase in plasma gastrin, the significant fall in gastric somatostatin levels and Bcl-2 protein expression and the rise in expression of COX-2 and Bax proteins. These mucosal changes were counteracted by the triple therapy and Lacidofil.

Conclusions: H. pylori-infection in gerbils, associated with regenerative hyperplasia of glandular structure, results in the suppression of gastric secretion, overexpression of COX-2 and enhancement in apoptosis and impairment of both, GBF and gastrin-somatostatin link which were reversed by anti- H. pylori triple therapy and attenuated by probiotics.