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

被引:10
作者
Matsushima, Y
Kinoshita, Y
Watanabe, M
Hassan, S
Fukui, H
Maekawa, T
Okada, A
Kawanami, C
Kishi, K
Watanabe, N
Nakao, M
Chiba, T
机构
[1] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, Kyoto 60601, Japan
[2] Kobe Univ Allied Med Sci, Dept Pathol, Kobe, Hyogo, Japan
[3] Takeda Chem Ind Ltd, Pharmaceut Res Labs 3, Osaka 532, Japan
关键词
Helicobacter felis; gastric mucosal lesion; stress; interleukin-1; beta; hepatocyte growth factor;
D O I
10.1159/000007586
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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-1 beta (IL-1 beta) 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-1 beta 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-1 beta mRNA. H. felis infection evoked enhanced expression of IL-1 beta 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-1 beta 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.
引用
收藏
页码:34 / 40
页数:7
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