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肥胖、先天免疫与肠道炎症。

Obesity, innate immunity and gut inflammation.

作者信息

Karagiannides Iordanes, Pothoulakis Charalabos

机构信息

Gastrointestinal Neuropeptide Center, Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

出版信息

Curr Opin Gastroenterol. 2007 Nov;23(6):661-6. doi: 10.1097/MOG.0b013e3282c8c8d3.

Abstract

PURPOSE OF REVIEW

The purpose of this review is to present recent data on how obesity-associated conditions may affect innate immunity and its role in the development of gut inflammation.

RECENT FINDINGS

Here we present studies that demonstrate the participation of adipose tissue components in the generation of inflammation. More specifically, we describe increases in the release of proinflammatory cytokines during obesity as well as the expression of receptors involved in innate immune responses by adipocytes. Furthermore, we present data on the involvement of adipose tissue-specific molecules (adipokines) in the generation of an environment that is favorable for diseases with an immune cause and in some cases (leptin) directly contribute to the development of inflammatory bowel disease. Finally, we present evidence supporting a putative association between obesity and gut inflammation through the link of inflammation with angiogenesis and neovascularization and the favorable conditions created for these responses in obesity.

SUMMARY

We believe that obesity-related systemic changes may create conditions that predispose to the development of gut inflammation or even worsen the progression of ongoing disease.

摘要

综述目的

本综述旨在介绍有关肥胖相关病症如何影响固有免疫及其在肠道炎症发展中作用的最新数据。

最新发现

在此,我们展示了一些研究,这些研究证明了脂肪组织成分参与炎症的产生。更具体地说,我们描述了肥胖期间促炎细胞因子释放的增加以及脂肪细胞中参与固有免疫反应的受体的表达。此外,我们展示了关于脂肪组织特异性分子(脂肪因子)参与营造有利于免疫源性疾病的环境的数据,并且在某些情况下(瘦素)直接促成炎症性肠病的发展。最后,我们提供证据支持肥胖与肠道炎症之间通过炎症与血管生成和新生血管形成的联系以及肥胖为这些反应创造的有利条件所建立的假定关联。

总结

我们认为,与肥胖相关的全身变化可能会创造条件,使个体易患肠道炎症,甚至会加剧现有疾病的进展。

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