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脂肪细胞因子在特发性炎症性肠病发病机制中的作用。

Adipokines in the pathogenesis of idiopathic inflammatory bowel disease.

机构信息

Health Promotion and Obesity Management Unit, Department of Pathophysiology, Medical University of Silesia, Katowice, Poland.

出版信息

Endokrynol Pol. 2013;64(3):226-31.

Abstract

Crohn's disease (CD) and ulcerative colitis (UC) are the two common forms of idiopathic inflammatory bowel disease (IBD). The aetiology and pathogenesis of IBD are not yet known. Genetic predisposition has been suggested as playing a role in the improper immune response to commensal microbiota. The main link of IBD pathogenesis is an intestinal immune system disability after enteric infection, resulting in an uncontrolled and chronic inflammatory state. Recently, numerous studies have been focused on the role of proinflammatory cytokines as well as hormones of adipose tissue named adipokines in the pathogenesis of IBD. Adipokines have pro- and anti-inflammatory properties and can modulate the immune response. It has been shown that obesity is associated with systemic microinflammation. On the other hand, experimental studies have revealed a link between levels of some adipokines and the severity of inflammation in IBD independent of body mass. The fat deposits called 'wrapping' or 'creeping' fat envelop the intestine, and adipokines produced by this tissue play an important role in the pathogenesis of IBD. The aim of this manuscript was to review the current literature concerning the role of adipokines in the pathogenesis of IBD.

摘要

克罗恩病(CD)和溃疡性结肠炎(UC)是两种常见的特发性炎症性肠病(IBD)。IBD 的病因和发病机制尚不清楚。遗传易感性被认为在对共生微生物群落的免疫反应异常中起作用。IBD 发病机制的主要环节是肠内感染后肠道免疫系统功能障碍,导致不受控制的慢性炎症状态。最近,许多研究集中在促炎细胞因子以及脂肪组织命名的脂肪细胞因子在 IBD 发病机制中的作用。脂肪细胞因子具有促炎和抗炎特性,可以调节免疫反应。已经表明肥胖与全身微炎症有关。另一方面,实验研究表明,一些脂肪细胞因子的水平与 IBD 炎症的严重程度有关,而与体重无关。称为“包裹”或“爬行”的脂肪沉积物包裹着肠道,这种组织产生的脂肪细胞因子在 IBD 的发病机制中起着重要作用。本文的目的是综述有关脂肪细胞因子在 IBD 发病机制中的作用的现有文献。

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