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性别对小鼠模型中猫幽门螺杆菌介导的胃炎、上皮细胞增殖和凋亡的影响。

The effect of gender on Helicobacter felis-mediated gastritis, epithelial cell proliferation, and apoptosis in the mouse model.

作者信息

Court M, Robinson P A, Dixon M F, Jeremy A H T, Crabtree J E

机构信息

Molecular Medicine Unit, St James's University Hospital, Leeds, UK.

出版信息

J Pathol. 2003 Oct;201(2):303-11. doi: 10.1002/path.1422.

Abstract

The murine Helicobacter felis model has been extensively used to investigate the importance of host factors in the development of chronic gastritis. The effect of gender in this murine model is unknown. Male and female C57BL/6J mice were infected with H felis for up to 1 year. At 4, 8, 19, 36, and 52 weeks post-infection, gastric histopathology, epithelial cell proliferation, and apoptosis were examined and compared with age- and gender-matched controls. In female mice, infection with H felis resulted in an earlier onset of chronic gastric inflammation, epithelial hyperplasia, and oxyntic cell loss than males. In females, there was a trend towards increased gastric pathology compared with males, with long-term-infected female mice having significantly greater (p < 0.05) chronic inflammation than male mice. The histopathological differences in male and female mice did not relate to the density of H felis infection. Female mice infected with H felis had significantly increased gastric epithelial cell proliferation in the cardia and corpus at both 8 and 52 weeks post-infection (p < 0.05). Epithelial cell apoptosis in the glandular mucosa of the corpus at 36 and 52 weeks post-infection was significantly increased (p < 0.05) in female mice compared with uninfected gender controls. In contrast, there was no significant increase in epithelial cell proliferation or apoptosis in any area of the stomach at any time point after H felis infection in male mice. These results demonstrate that there are gender differences in the gastric inflammatory and epithelial response to H felis in the murine model. The functional importance of gender should be considered in future murine studies on H felis- and H pylori-induced chronic gastritis.

摘要

小鼠幽门螺杆菌模型已被广泛用于研究宿主因素在慢性胃炎发展中的重要性。在这个小鼠模型中,性别因素的影响尚不清楚。将雄性和雌性C57BL/6J小鼠感染幽门螺杆菌长达1年。在感染后4周、8周、19周、36周和52周,检查胃组织病理学、上皮细胞增殖和凋亡情况,并与年龄和性别匹配的对照组进行比较。在雌性小鼠中,感染幽门螺杆菌导致慢性胃炎、上皮增生和泌酸细胞丢失的发病时间比雄性小鼠更早。与雄性相比,雌性小鼠的胃部病理学有加重趋势,长期感染的雌性小鼠的慢性炎症明显比雄性小鼠更严重(p<0.05)。雄性和雌性小鼠的组织病理学差异与幽门螺杆菌感染密度无关。感染幽门螺杆菌的雌性小鼠在感染后8周和52周时,贲门和胃体部的胃上皮细胞增殖明显增加(p<0.05)。与未感染的性别匹配对照组相比,感染后36周和52周时,雌性小鼠胃体部腺黏膜的上皮细胞凋亡明显增加(p<0.05)。相比之下,雄性小鼠在感染幽门螺杆菌后的任何时间点,胃的任何区域的上皮细胞增殖或凋亡均无明显增加。这些结果表明,在小鼠模型中,胃对幽门螺杆菌的炎症和上皮反应存在性别差异。在未来关于幽门螺杆菌和幽门螺旋杆菌诱导的慢性胃炎的小鼠研究中,应考虑性别的功能重要性。

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