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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Citrobacter rodentium infection causes iNOS-independent intestinal epithelial dysfunction in mice.
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Citrobacter rodentium infection causes iNOS-independent intestinal epithelial dysfunction in mice.

机译：啮齿动物柠檬酸杆菌感染会在小鼠中引起iNOS依赖性肠上皮功能障碍。

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摘要

Attaching-effacing bacteria are major causes of infectious diarrhea in humans worldwide. Citrobacter rodentium is an attaching-effacing enteric pathogen that causes transmissible murine colonic mucosal hyperplasia. We characterized colonic inflammation and ion transport at 3, 7, 10, 30, and 60 d after infection of C57Bl/6 mice with C. rodentium. Macroscopic damage score was significantly increased 7 and 10 d after infection. Colonic wall thickness was increased at 7, 10, 30, and 60 d. Myeloperoxidase (MPO) activity was significantly increased at 3, 7, and 10 d and returned to control levels by days 30 and 60. The expressions of inducible nitric oxide synthase and cyclooxygenase-2 were increased by C. rodentium infection. Significant reductions in the epithelial secretory response to carbachol, but not to electrical field stimulation or forskolin, were observed at 3 and 10 d of infection. Translocation of enteric bacteria into the mesenteric lymph nodes was observed 10 d following infection. There was no difference in response to infection between animals deficient in inducible nitric oxide synthase and wild-type controls. The COX-2 inhibitor rofecoxib caused decreased wall thickness and MPO activity at day 10. However, COX-2 inhibition did not alter infection-induced changes in ion transport. Citrobacter rodentium infection causes colonic inflammation, mucosal hyperplasia, and nitric-oxide-independent epithelial dysfunction in association with increased permeability to luminal bacteria.
机译：附着细菌是全世界人类感染性腹泻的主要原因。啮齿类柠檬酸杆菌是一种附着在表面的肠道病原体，可导致鼠类结肠结肠黏膜增生传播。我们表征了C.Bl / 6小鼠感染了C.rodentium后第3、7、10、30和60 d的结肠炎症和离子转运。感染后7和10 d，肉眼可见的损伤评分显着增加。结肠壁厚度在第7、10、30和60 d增加。髓过氧化物酶（MPO）活性在第3、7和10 d显着增加，并在第30和60天恢复到对照水平。C。rodentium感染使诱导型一氧化氮合酶和环氧合酶2的表达增加。在感染后第3天和第10天观察到对卡巴胆碱的上皮分泌反应显着降低，但对电场刺激或福司可林则没有。感染后10 d观察到肠道细菌易位进入肠系膜淋巴结。缺乏可诱导型一氧化氮合酶的动物与野生型对照之间对感染的反应没有差异。在第10天，COX-2抑制剂rofecoxib导致壁厚降低和MPO活性降低。但是，COX-2抑制剂并未改变感染引起的离子转运变化。啮齿动物柠檬酸杆菌感染会导致结肠炎症，粘膜增生和非一氧化氮非依赖性上皮功能障碍，并增加对腔内细菌的渗透性。

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