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      Augmentation of water-immersion stress- induced gastric mucosal lesions in BALB/c mice infected with Helicobacter felis.

      Digestion
      Animals, Blotting, Northern, Female, Gastric Mucosa, pathology, Gastritis, microbiology, physiopathology, Helicobacter, pathogenicity, Helicobacter Infections, Hepatocyte Growth Factor, biosynthesis, Immersion, Interleukin-1, Mice, Mice, Inbred BALB C, RNA, Messenger, genetics, Stomach Ulcer, Stress, Physiological, Time Factors

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          Abstract

          Inoculation of Helicobacter felis into the murine stomach has been reported to induce chronic gastric inflammation and may be a model of Helicobacter pylori-induced chronic gastritis. In this study, to characterize H. felis-induced gastritis, the gastric production of interleukin-1beta (IL-1beta) and hepatocyte growth factor (HGF) was measured in mice. Gastric mucosal lesions were induced in H. felis-infected BALB/c mice by water-immersion stress. The severity score of gastric erosions per stomach was measured as the sum of the length of erosions. Gene expression of IL-1beta and HGF were analyzed by Northern blot analysis and production of HGF was examined using the enzyme immunoassay method. Water-immersion stress induced gastric mucosal lesions accompanied by increased expression of IL-1beta mRNA. H. felis infection evoked enhanced expression of IL-1beta and HGF genes. When H. felis-infected mice were stressed by water immersion, the mucosal lesions were more severe than those in non-infected mice. Moreover, IL-1beta gene expression as well as HGF production was further increased. Although H. felis inoculation did not cause gastric mucosal erosions by itself, it augmented the stress-induced erosions.

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