大肠杆菌
免疫学
免疫系统
巨噬细胞
病理生理学
克罗恩病
炎症性肠病
疾病
病因学
生物
微生物学
医学
基因
病理
遗传学
体外
作者
Anthony Buisson,Marie-Agnès Bringer,Nicolas Barnich,Emilie Vazeille
出处
期刊:Inflammatory Bowel Diseases
[Oxford University Press]
日期:2016-11-02
卷期号:22 (12): 2943-2955
被引量:10
标识
DOI:10.1097/mib.0000000000000946
摘要
The pathophysiology of Crohn's disease (CD), a chronic inflammatory bowel disease, remains imperfectly elucidated. Consequently, the therapeutic armamentarium remains limited and has not changed the natural history of CD hitherto. Accordingly, physicians need to identify new therapeutic targets to be able to alter the intestinal damage. The most recent hypothesis considered CD as resulting from an abnormal interaction between microbiota and host immune system influenced by genetics and environmental factors. Several experimental and genetic evidence point out intestinal macrophages in CD etiology. An increase of macrophages number and the presence of granulomas are especially observed in the intestinal mucosa of patients with CD. These macrophages could be defective and particularly in responses to infectious agents like CD-associated Escherichia coli. This review focuses on, what is currently known regarding the role of macrophages, macrophages/E. coli interaction, and the impact of CD therapies on macrophages in CD. We also speculate that macrophages modulation could lead to important translational implications in CD with the end goal of promoting gut health.
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