Atrophic gastric changes in both Helicobacter felis and Helicobacter pylori infected mice are host dependent and separate from antral gastritis.

Abstract

Results-In SJL, C3H/He, DBA/2, and C57BIJ6 infected mice, severe to moderlate chronic active gastritis was observed only in the body of the stomach, which increased in severity over time with specialised cells in the body glands being replaced. As the severity of this damage in the body increased and atrophic changes were seen, the level of bacterial colonisation of the antrum decreased. In contrast, in BALB/c and CBA mice, there was only mild gastritis in the antrum, no remarkable changes were detected in their body mucosa, and no atrophy was seen over time. In both these strains of mice, heavy bacterial colonisation was seen, which tended to increase over the period of the experiment. Of particular importance in this experiment was that bacterial colonisation was mainly restricted to the antrum yet the atrophy, when present, was only observed in the body of the stomach. H pyloni infected C3HIHe mice showed moderate colonisation of the antrum, which persisted up to six months with little development of atrophy. In contrast, H pylorn in C57BL/6 mice showed excellent colonisation of the antrum at two months but six months after infection there was moderate to severe body atrophy, which was associated with a loss of bacteria from the antrum. Conclusions-These findings challenge current concepts of the development of Helicobacter induced atrophy in that active chronic gastritis of antrum or the body mucosa, or both, is not a prerequisite. They also suggest an autoimmune basis for the pathology although no autoantibody or antibody to the H'IK' ATPase was detected. Loss of infecting helicobacters from the stomach together with development of an atrophic gastritis in the body ofthe stomach is similar to the pattern found in certain H pylori infected human subjects.

RAPD-PCR, Histopathological and Serological Analysis of Four Mouse Strains Infected with Multiple Strains ofHelicobacter pylori

“…Thus, the isolate 119/95, which became predominant in mice, does not seem to be host-dependent in the mice investigated. However, Sakagami et al (25) reported that both C3H/He and C57BL/6 mice exhibited a more severe inflammation by H. felis and H. pylori infection in these inbred strains of mice. Lee et al (19) also reported differences in host response in inflammation and colonisation.…”

Immunogenetic analysis of gastric MALT lymphoma-like lesions induced by Helicobacter pylori infection in neonatally thymectomized mice

“…Moreover, lymphoid follicle formation by H. pylori infection was never observed in C57BL/6J mice irrespective of nTx, although these mice developed severe active gastritis by H. pylori infection, which is believed to be a typical Th1-type inflammation (data not shown). [24][25][26] These data suggest that, in contrast to H. pylori-induced active gastritis, both Th1 and Th2 responses are necessary for the development of MALT lymphomalike lesions by H. pylori infection. Supporting this idea, we observed, in addition to IFN-g, expression of IL-4, a representative Th2-type cytokine, in the gastric mucosa of only H. pylori-infected BALB/c mice with nTx that developed lymphoid follicles.…”

Pitavastatin Fails to Lower Serum Lipid Levels or Inhibit Gastric Carcinogenesis in Helicobacter pylori–Infected Rodent Models

“…Because cytochrome P450 metabolisms in gerbils have not been fully clarified yet, we selected pitavastatin to avoid species difference in the drug metabolism in this experiment. Among mice strains, C57BL/6 mice showed excellent colonization of H. pylori in the antrum, whereas BALB/c and CBA mice showed only mild gastritis (35); thus, the former was chosen here. Pitavastatin has been shown to prevent digestive system carcinogenesis, such as colorectal and lingual cancer, in mouse models (14, 36); however, the degree of gastritis in our study was not attenuated by pitavastatin in H. pylori-infected gerbils and mice.…”