| 特集名 | 胃癌のリスクファクター | |
|---|---|---|
| 題名 | 微生物 (3) H.pylori感染と食塩 -- 胃炎・胃粘膜萎縮との関わりについて | |
| 発刊年月 | 2004年 03月 | |
| 著者 | 谷中 昭典 | 筑波大学臨床医学系消化器内科 |
| 著者 | 張 松華 | 筑波大学臨床医学系消化器内科 |
| 著者 | 田内 雅史 | 筑波大学臨床医学系消化器内科 |
| 著者 | 鈴木 英雄 | 筑波大学臨床医学系消化器内科 |
| 著者 | 柴原 健 | 筑波大学臨床医学系消化器内科 |
| 著者 | 松井 裕史 | 筑波大学臨床医学系消化器内科 |
| 著者 | 中原 朗 | 筑波大学臨床医学系消化器内科 |
| 著者 | 田中 直見 | 筑波大学臨床医学系消化器内科 |
| 【 要旨 】 | 【目的】Helicobacter pylori (H.pylori) 以外の胃癌発症因子として，食塩の関与が指摘されている．本研究では，食塩摂取がH.pylori感染胃粘膜に及ぼす影響，およびその機序をH.pylori感染マウスを用いて検討した．【方法】C57BL/6マウスをH.pylori感染群とH.pylori感染群に分け，各群に対して高塩分食 (7.5％NaCl) あるいは対照食 (0.25％NaCl) を2カ月間摂取させた後，胃粘膜を摘出し，胃粘膜の組織学的変化，酸分泌能，胃粘膜細胞のアポトーシス，胃粘膜IL-1beta，IL-8，PGE2産生能を検討した．同一の実験をIL-1受容体欠損マウス，野生型マウス両方で行い，それぞれのマウスより得られた成績を比較した．【成績】(1) 高塩分食は，とくに野生型マウス，H.pylori感染群の胃酸分泌能を低下させ，胃体部粘膜におけるIL-1beta，IL-8，COX-2の発現を増強し，上皮細胞のアポトーシスを亢進させ，胃体部粘膜萎縮の進展を加速した．(2) IL-1受容体欠損マウスでは高塩分食による上記の胃粘膜変化は，H.pylori感染群，H.pylori非感染群ともにきわめて軽度であった．【結論】高塩分食は，一つの機序としてIL-1betaの発現を増強することによりH.pylori感染マウスの胃粘膜萎縮の進展を加速させることが示唆された． | |
| Theme | Risk Factors for Gastric Carcinogenesis | |
|---|---|---|
| Title | Role of Helicobacter pylori Infection and High Salt Diet in Progression of Gastric Atrophy in Mice | |
| 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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