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黏液素在生理和病理条件下的动态变化。

Mucins Dynamics in Physiological and Pathological Conditions.

机构信息

Department of Biomedicine, University of Basel, 4031 Basel, Switzerland.

Roche Pharma Research & Early Development, Immunology, Infectious Diseases and Ophthalmology (I2O), Roche Innovation Center, 4031 Basel, Switzerland.

出版信息

Int J Mol Sci. 2021 Dec 20;22(24):13642. doi: 10.3390/ijms222413642.

DOI:10.3390/ijms222413642
PMID:34948435
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8707880/
Abstract

Maintaining intestinal health requires clear segregation between epithelial cells and luminal microbes. The intestinal mucus layer, produced by goblet cells (GCs), is a key element in maintaining the functional protection of the epithelium. The importance of the gut mucus barrier is highlighted in mice lacking , the major form of secreted mucins. These mice show closer bacterial residence to epithelial cells, develop spontaneous colitis and became moribund when infected with the attaching and effacing pathogen, . Furthermore, numerous observations have associated GCs and mucus layer dysfunction to the pathogenesis of inflammatory bowel disease (IBD). However, the molecular mechanisms that regulate the physiology of GCs and the mucus layer remain obscured. In this review, we consider novel findings describing divergent functionality and expression profiles of GCs subtypes within intestinal crypts. We also discuss internal (host) and external (diets and bacteria) factors that modulate different aspects of the mucus layer as well as the contribution of an altered mucus barrier to the onset of IBD.

摘要

维持肠道健康需要明确分隔上皮细胞和腔微生物。由杯状细胞(GCs)产生的肠道粘液层是维持上皮功能保护的关键因素。在缺乏主要分泌粘蛋白的小鼠中,肠道粘液屏障的重要性得到了强调。这些小鼠表现出更接近上皮细胞的细菌驻留,自发发生结肠炎,并在感染附着和消蚀病原体时变得病危。此外,许多观察结果将 GCs 和粘液层功能障碍与炎症性肠病(IBD)的发病机制联系起来。然而,调节 GCs 和粘液层生理学的分子机制仍然不清楚。在这篇综述中,我们考虑了描述肠道隐窝中 GCs 亚型不同功能和表达谱的新发现。我们还讨论了调节粘液层不同方面的内部(宿主)和外部(饮食和细菌)因素,以及改变的粘液屏障对 IBD 发病的贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/477c/8707880/d3c38a4fc72e/ijms-22-13642-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/477c/8707880/c2223ebf9db6/ijms-22-13642-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/477c/8707880/b4d205f77383/ijms-22-13642-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/477c/8707880/b796bb0a94f5/ijms-22-13642-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/477c/8707880/d3c38a4fc72e/ijms-22-13642-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/477c/8707880/c2223ebf9db6/ijms-22-13642-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/477c/8707880/b4d205f77383/ijms-22-13642-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/477c/8707880/b796bb0a94f5/ijms-22-13642-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/477c/8707880/d3c38a4fc72e/ijms-22-13642-g004.jpg

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