High-salt diet induces gastric epithelial hyperplasia and parietal cell loss, and enhances Helicobacter pylori colonization in C57BL/6 mice.
High-salt diet induces gastric epithelial hyperplasia and parietal cell loss, and enhances Helicobacter pylori colonization in C57BL/6 mice.
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发表时间：
1999-10
期刊：
影响因子：
11.2
通讯作者：
J. Fox;C. Dangler;N. Taylor;Amy King;T. Koh;T. Wang
中科院分区：
文献类型：
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作者：
J. Fox;C. Dangler;N. Taylor;Amy King;T. Koh;T. Wang
已知人类和实验动物的高盐饮食会引起胃炎，与萎缩性胃炎的高风险相关，并被认为是胃肿瘤的促进剂。在实验室啮齿类动物中，已知盐会引起胃炎，当同时给药时，它会促进已知胃致癌物的致癌作用。由于幽门螺杆菌与从胃炎到胃癌的进展有关，我们设计了一项研究，以确定过量的饮食NaCl是否会对H.幽门感染72只8周龄雌性C57 BL/6小鼠感染H. pylori菌株Sydney，36只对照小鼠仅给予载体。在给药前2周和整个实验期间，对一半的感染小鼠和对照小鼠饲喂高盐饮食（7.5% vs 0.25%）。在第4、8和16周，对来自高盐饮食组和正常饮食组的12只感染动物和6只对照动物实施安乐死。在感染后8周和16周，高盐饮食组动物的胃体和胃窦中每克组织的菌落形成单位显著高于正常饮食组（P < 0.05）。与对照组相比，高盐饮食组动物胃体和胃窦中的定量尿素酶在4和8 WPI时显著升高（P < 0.05）。在16 WPI时，正常和高盐饮食组的小鼠对H.幽门感染然而，高盐饮食小鼠胃粘膜体的胃小凹被拉长并被H.幽门螺杆菌的发生率高于正常饮食的小鼠。高盐饮食还与近端体和胃窦的增殖显著增加以及近端体壁细胞数量的多灶性减少相关，导致胃小凹延长。我们的结论是，过量的NaCl摄入增强H。幽门螺杆菌在小鼠和人类中的定植以及慢性盐摄入可能通过增加H.幽门定植。此外，盐摄入量增加可能会增强H。幽门相关癌通过诱导增殖、小凹细胞增生和腺萎缩而发生。
A high-salt diet in humans and experimental animals is known to cause gastritis, has been associated with a high risk of atrophic gastritis, and is considered a gastric tumor promoter. In laboratory rodents, salt is known to cause gastritis, and when coadministered, it promotes the carcinogenic effects of known gastric carcinogens. Because Helicobacter pylori has been associated with a progression from gastritis to gastric cancer, we designed a study to determine whether excessive dietary NaCl would have an effect on colonization and gastritis in the mouse model of H. pylori infection. Seventy-two, 8-week-old female C57BL/6 mice were infected with H. pylori strain Sydney, and 36 control mice were dosed with vehicle only. One-half of the infected and control mice were fed a high-salt diet (7.5% versus 0.25%) for 2 weeks prior to dosing and throughout the entire experiment. Twelve infected and 6 control animals from the high-salt and normal diet groups were euthanized at 4, 8, and 16 weeks. At 8 and 16 weeks postinfection (WPI), the colony-forming units per gram of tissue were significantly higher (P < 0.05) in the corpus and antrum of animals in the high-salt diet group compared with those on the normal diet. Quantitative urease was significantly higher (P < 0.05) at 4 and 8 WPI in the corpus and antrum of animals on the high-salt diet when compared with controls. At 16 WPI, mice in both the normal and the high-salt diet groups developed moderate to marked atrophic gastritis of the corpus in response to H. pylori infection. However, the gastric pits of the corpus mucosa in mice on the high-salt diet were elongated and colonized by H. pylori more frequently than those in mice on the normal diet. The high-salt diet was also associated with a significant increase in proliferation in the proximal corpus and antrum and a multifocal reduction in parietal cell numbers in the proximal corpus, resulting in the elongation of gastric pits. We conclude that excessive NaCl intake enhances H. pylori colonization in mice and in humans and that chronic salt intake may exacerbate gastritis by increasing H. pylori colonization. Furthermore, elevated salt intake may potentiate H. pylori-associated carcinogenesis by inducing proliferation, pit cell hyperplasia, and glandular atrophy.