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Augmentation of Water-Immersion Stress- Induced Gastric Mucosal Lesions in BALB/c Mice Infected with Helicobacter felis

Matsushima Y.a · Kinoshita Y.b · Watanabe M.c · Hassan S.a · Fukui H.a · Maekawa T.a · Okada A.a · Kawanami C.a · Kishi K.a · Watanabe N.a · Nakao M.d · Chiba T.a
aDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, b2nd Division of Internal Medicine, Shimane, cDepartment of Pathology, Kobe University of Allied Medical Sciences, Kobe, and dPharmaceutical Research Laboratories III, Takeda Chemical Industries, Ltd., Osaka, Japan Digestion 1999;60:34–40 (DOI:10.1159/000007586)

Abstract

Background and Aims: 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-1β (IL-1β) and hepatocyte growth factor (HGF) was measured in mice. Methods: 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-1β and HGF were analyzed by Northern blot analysis and production of HGF was examined using the enzyme immunoassay method. Results: Water-immersion stress induced gastric mucosal lesions accompanied by increased expression of IL-1β mRNA. H. felis infection evoked enhanced expression of IL-1β 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-1β gene expression as well as HGF production was further increased. Conclusions: Although H. felis inoculation did not cause gastric mucosal erosions by itself, it augmented the stress-induced erosions.

 

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