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首页> 外文期刊>The Journal of toxicological sciences >Metallothionein deficiency exacerbates chronic inflammation associated with carcinogenesis in stomach of mice infected with Helicobacter pylori.
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Metallothionein deficiency exacerbates chronic inflammation associated with carcinogenesis in stomach of mice infected with Helicobacter pylori.

机译：金属硫蛋白缺乏症加剧了幽门螺杆菌感染小鼠胃癌的慢性炎症。

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摘要

Metallothionein (MT), a low-molecular-weight protein with a high affinity for divalent heavy metal ions, is involved in many pathophysiological processes, including metal homeostasis, detoxification, cell proliferation and protection against oxidative damage. We previously found that MT in gastric mucosa plays a role in protecting against Helicobacter pylori (H. pylori)-induced gastritis at the early stage of infection. H. pylori-induced chronic gastric inflammation is shown to be associated with gastric carcinogenesis. Thus, to examine whether gastric MT contributes to protection against H. pylori-induced chronic inflammation, we compared histological changes in the gastric mucosa of MT-null and the wild-type mice at 53 weeks after inoculation three times with H. pylori SS1. As a result, we observed disruption of the gastric mucosa in MT-null mice, but not in the wild-type mice, even at the late stage of H. pylori-infection. Evaluation of pathological changes in gastric specimens by the updated Sydney grading system revealed that scores related to chronic inflammation and polymorphonuclear cell activity were higher in infected MT-null mice than those in the wild-type mice. Furthermore, a higher score for metaplasia was also observed in the MT-null stomach. These results suggested that MT might be involved in protecting against H. pylori-induced gastric chronic inflammation associated with carcinogenesis.
机译：金属硫蛋白（MT）是一种对二价重金属离子具有高亲和力的低分子量蛋白质，它参与许多病理生理过程，包括金属稳态，解毒，细胞增殖和抗氧化损伤。我们先前发现，胃粘膜中的MT在感染的早期阶段起着防御幽门螺杆菌（H. pylori）诱导的胃炎的作用。幽门螺杆菌诱导的慢性胃炎症与胃癌发生有关。因此，为了检查胃MT是否有助于预防幽门螺杆菌引起的慢性炎症，我们比较了在接种幽门螺杆菌SS1 3次后53周，MT空小鼠和野生型小鼠的胃黏膜的组织学变化。结果，即使在幽门螺杆菌感染的后期，我们也观察到MT无效小鼠的胃粘膜破坏，而野生型小鼠则没有。通过更新的悉尼分级系统对胃标本的病理变化进行评估后发现，感染MT的小鼠中与慢性炎症和多形核细胞活性相关的得分要高于野生型小鼠。此外，在无MT的胃中也观察到了较高的生化评分。这些结果表明MT可能参与预防幽门螺杆菌诱导的与癌变有关的胃慢性炎症。

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