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白细胞介素-13 介导的肠道嗜铬细胞增生和血清素产生的免疫控制。

IL-13-mediated immunological control of enterochromaffin cell hyperplasia and serotonin production in the gut.

机构信息

Farncombe Family Digestive Health Research Institute, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.

出版信息

Mucosal Immunol. 2013 Jan;6(1):146-55. doi: 10.1038/mi.2012.58. Epub 2012 Jul 4.

Abstract

Enterochromaffin (EC) cells in the gastrointestinal (GI) mucosa are the main source of serotonin (5-hydroxytryptamine (5-HT)) in the body. 5-HT is implicated in the pathophysiology of many GI disorders including functional and inflammatory bowel disorders. Herein we studied the role of interleukin 13 (IL-13) in EC cell biology by utilizing IL-13-deficient (IL-13-/-) mice and BON cells (a model for human EC cells). The numbers of EC cells and 5-HT amount were significantly lower in enteric parasite, Trichuris muris-infected IL-13-/- mice compared with the wild-type mice. This was accompanied with increased parasite burden in IL-13-/- mice. Treatment of naive and infected IL-13-/- mice with IL-13 increased EC cell numbers and 5-HT amount. BON cells expressed IL-13 receptor and in response to IL-13 produced more 5-HT. These results provide novel information on IL-13-mediated immunological control of 5-HT in the gut, which may ultimately lead to improved therapeutic opportunities in various GI disorders.

摘要

肠嗜铬(EC)细胞是体内 5-羟色胺(5-HT)的主要来源。5-HT 与许多胃肠道疾病的病理生理学有关,包括功能性和炎症性肠病。在这里,我们通过利用白细胞介素 13(IL-13)缺陷(IL-13-/-)小鼠和 BON 细胞(一种人类 EC 细胞模型)研究了白细胞介素 13 在 EC 细胞生物学中的作用。与野生型小鼠相比,肠道寄生虫旋毛虫感染的 IL-13-/-小鼠的 EC 细胞数量和 5-HT 含量明显降低。这伴随着 IL-13-/-小鼠中寄生虫负担的增加。用 IL-13 治疗未感染和感染的 IL-13-/-小鼠可增加 EC 细胞数量和 5-HT 含量。BON 细胞表达 IL-13 受体,并对 IL-13 产生更多的 5-HT。这些结果提供了关于 IL-13 介导的肠道 5-HT 免疫控制的新信息,这可能最终为各种胃肠道疾病提供更好的治疗机会。

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