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肠道屏障功能与炎症中的微绒毛间黏附复合体

The intermicrovillar adhesion complex in gut barrier function and inflammation.

作者信息

Mödl Bernadette, Schmidt Katy, Moser Doris, Eferl Robert

机构信息

Center for Cancer Research, Medical University of Vienna & Comprehensive Cancer Center, 1090 Vienna, Austria.

Division of Cell and Developmental Biology, Medical University of Vienna, 1090 Vienna, Austria.

出版信息

Explor Dig Dis. 2022 Oct 11;1:72-79. doi: 10.37349/edd.2022.00006.

DOI:10.37349/edd.2022.00006
PMID:39092422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7616328/
Abstract

The surface of intestinal epithelial cells is covered by the brush border, which consists of densely packed cellular extrusions called microvilli. Until recently, microvilli have not been known to be interconnected. In 2014, a protein complex, called the intermicrovillar adhesion complex (IMAC) which is located at the tips of the microvilli and responsible for the regular spatial organization of the brush border, was identified. Deletion of IMAC components such as cadherin-related family member-2 (CDHR2) in mice resulted in microvillus disorganization and fanning, a structural aberration that is also found in the brush border of patients with inflammatory bowel disease. The etiology of inflammatory bowel disease has been primarily associated with dysfunctional mucosal immunity, but the discovery of the IMAC may encourage theories of an epithelial origin. Here, possible effects of the brush border on the gut barrier function and intestinal inflammation are discussed proposing that the IMAC protects against inflammation through its microvillus cross-linking function.

摘要

肠道上皮细胞的表面覆盖着刷状缘,它由密集排列的细胞突起即微绒毛组成。直到最近,人们还不知道微绒毛是相互连接的。2014年,一种位于微绒毛顶端、负责刷状缘规则空间组织的蛋白质复合物——微绒毛间黏附复合物(IMAC)被发现。在小鼠中删除IMAC成分,如钙黏蛋白相关家族成员2(CDHR2),会导致微绒毛紊乱和扇形化,这种结构畸变也出现在炎症性肠病患者的刷状缘中。炎症性肠病的病因主要与黏膜免疫功能失调有关,但IMAC的发现可能会催生上皮起源的理论。在此,我们讨论了刷状缘对肠道屏障功能和肠道炎症的可能影响,提出IMAC通过其微绒毛交联功能预防炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04d/7616328/976a8d2dae85/EMS197458-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04d/7616328/68cc99ccddbc/EMS197458-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04d/7616328/877da65bd42b/EMS197458-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04d/7616328/976a8d2dae85/EMS197458-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04d/7616328/68cc99ccddbc/EMS197458-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04d/7616328/877da65bd42b/EMS197458-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04d/7616328/976a8d2dae85/EMS197458-f003.jpg

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Biomed Pharmacother. 2022 Feb;146:112543. doi: 10.1016/j.biopha.2021.112543. Epub 2021 Dec 20.
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Pathway paradigms revealed from the genetics of inflammatory bowel disease.从炎症性肠病的遗传学中揭示的途径范式。
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Host-microbiota interactions in inflammatory bowel disease.
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