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肠道炎症期间结肠M细胞的诱导

Induction of Colonic M Cells during Intestinal Inflammation.

作者信息

Bennett Kaila M, Parnell Erinn A, Sanscartier Candice, Parks Sophia, Chen Gang, Nair Meera G, Lo David D

机构信息

Bioengineering Interdepartmental Graduate Program, School of Medicine, University of California, Riverside, Riverside, California; Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California.

Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California.

出版信息

Am J Pathol. 2016 May;186(5):1166-79. doi: 10.1016/j.ajpath.2015.12.015. Epub 2016 Mar 3.

DOI:10.1016/j.ajpath.2015.12.015
PMID:26948422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4861757/
Abstract

Intestinal M (microfold) cells are specialized epithelial cells overlying lymphoid tissues in the small intestine. Unlike common enterocytes, M cells lack an organized apical brush border, and are able to transcytose microparticles across the mucosal barrier to underlying antigen-presenting cells. We found that in both the dextran sodium sulfate and Citrobacter rodentium models of colitis, significantly increased numbers of Peyer's patch (PP) phenotype M cells were induced at the peak of inflammation in colonic epithelium, often accompanied by loosely organized lamina propria infiltrates. PP type M cells are thought to be dependent on cytokines, including tumor necrosis factor (TNF)-α and receptor activator of nuclear factor kappa-B ligand; these cytokines were also found to be induced in the inflamed tissues. The induction of M cells was abrogated by anti-TNF-α blockade, suggesting that anti-TNF-α therapies may have similar effects in clinical settings, although the functional consequences are not clear. Our results suggest that inflammatory cytokine-induced PP type M cells may be a useful correlate of chronic intestinal inflammation.

摘要

肠道M(微褶)细胞是覆盖在小肠淋巴组织上的特化上皮细胞。与普通肠上皮细胞不同,M细胞缺乏有组织的顶端刷状缘,并且能够跨细胞转运微粒穿过黏膜屏障至其下方的抗原呈递细胞。我们发现在葡聚糖硫酸钠和鼠柠檬酸杆菌结肠炎模型中,结肠上皮炎症高峰期诱导出的派尔集合淋巴结(PP)表型M细胞数量显著增加,常伴有固有层浸润组织松散。PP型M细胞被认为依赖于细胞因子,包括肿瘤坏死因子(TNF)-α和核因子κB受体激活剂配体;这些细胞因子在炎症组织中也被发现有诱导作用。抗TNF-α阻断可消除M细胞的诱导,这表明抗TNF-α疗法在临床环境中可能有类似作用,尽管其功能后果尚不清楚。我们的结果表明,炎症细胞因子诱导的PP型M细胞可能是慢性肠道炎症的一个有用相关指标。

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本文引用的文献

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