| Theme | Risk Factors for Gastric Carcinogenesis | |
|---|---|---|
| Title | Role of Helicobacter pylori Infection and High Salt Diet in Progression of Gastric Atrophy in Mice | |
| Publish Date | 2004/03 | |
| Author | Akinori Yanaka | Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba |
| Author | Songhua Zhang | Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba |
| Author | Masahumi Tauchi | Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba |
| Author | Hideo Suzuki | Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba |
| Author | Takeshi Shibahara | Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba |
| Author | Hirohumi Matsui | Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba |
| Author | Akira Nakahara | Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba |
| Author | Naomi Tanaka | Department of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba |
| [ Summary ] | A high Salt Diet Accelerates the Progression of the Atrophy of Helicobacter pylori-infected Gastric Corpus Mucosa in Wild Type C57/B6 Mice, but Not in LI-1 receptor Knockout Mice in vivo. This study was conducted to examine the mechanisms by which a high salt diet exaggerates gastritis, and accelerates the progression of atrophy in Hp-infected gastric corpus mucosa. Methods: Animal models of Hp infection were set up by inoculating C57BL/6 mice with the Hp Sydney Strain; mice were divided into 2 groups (Hp-negative vs Hp-positive), and each group was divided into two subgroups (control diet vs high salt diet). Mice were sacrificed at eight wks after treatment. Acid secretion, gastritis, atrophy, and apoptosis were analyzed. The same series of experiments was conducted in IL-1 receptor knockout (IL-1 R-/-) mice. Results were compared between the wild type C57BL6 (IL-1 R+/+) mice and the IL-1 R-/-mice. Results: 1. A high salt diet exacerbated inflammation, and enhanced apoptosis, especially in the corpus mucosa in Hp-infected in IL-1 R+/+, but not in IL-1 R-/-mice. 2. In IL-1 R+/+ Hp-infected mice. A high salt diet enhanced expression of IL-1b, IL-8, and COX-2 in the corpus mucosa and significantly reduced pentagastrin-stimulated acid secretion. These effects were abolished in IL-1 R-/-mice. Conclusion: The chronic intake of a high salt diet exacerbates corpus gastritis and accelerates the progression of atrophy in H.pylori-infected mice, the effects which were at least in part, mediated by enhancing induction of IL-1b. |
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