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胆汁酸受体调节肠道巨噬细胞在炎症性肠病中的作用。

Bile acid receptors regulate the role of intestinal macrophages in inflammatory bowel disease.

作者信息

Yang Hongjie, Shi Xianhong, Wang Beibei, Li Heng, Li Bin, Zhou Tianqi, Tian Lulu, Wang Shengjun, Yin Kai

机构信息

Department of General Surgery, Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, Jiangsu, China.

Department of Laboratory Medicine, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.

出版信息

Front Immunol. 2025 Jun 17;16:1577000. doi: 10.3389/fimmu.2025.1577000. eCollection 2025.

DOI:10.3389/fimmu.2025.1577000
PMID:40599770
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12208833/
Abstract

Many factors, including genetic vulnerability, barrier function, intestinal immune cells, and intestinal microbiota, may combine to affect the occurrence and progression of inflammatory bowel disease (IBD). Through targeting bile acid receptors (BARs), bile acids have been demonstrated to have a range of regulatory effects on intestinal immune responses in recent decades. As the basis of intestinal immunity, macrophages play an indispensable role in intestinal homeostasis. BARs connect the intestinal microbiota with immune cells, significantly impacting IBD. This review focuses on the role of bile acids in regulating the differentiation and function of intestinal macrophages in IBD.

摘要

包括遗传易感性、屏障功能、肠道免疫细胞和肠道微生物群在内的多种因素可能共同作用，影响炎症性肠病（IBD）的发生和发展。近几十年来，通过靶向胆汁酸受体（BARs），已证明胆汁酸对肠道免疫反应具有一系列调节作用。作为肠道免疫的基础，巨噬细胞在肠道稳态中发挥着不可或缺的作用。BARs将肠道微生物群与免疫细胞联系起来，对IBD产生显著影响。本综述重点关注胆汁酸在调节IBD中肠道巨噬细胞分化和功能方面的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/839eb63a2e3c/fimmu-16-1577000-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/e75f8551a413/fimmu-16-1577000-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/2ee228b42651/fimmu-16-1577000-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/173b5002472c/fimmu-16-1577000-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/6d295c7b56c6/fimmu-16-1577000-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/39c8bb8ca0b7/fimmu-16-1577000-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/839eb63a2e3c/fimmu-16-1577000-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/e75f8551a413/fimmu-16-1577000-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/2ee228b42651/fimmu-16-1577000-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/173b5002472c/fimmu-16-1577000-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/6d295c7b56c6/fimmu-16-1577000-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/39c8bb8ca0b7/fimmu-16-1577000-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f47/12208833/839eb63a2e3c/fimmu-16-1577000-g006.jpg

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本文引用的文献

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Biomed Pharmacother. 2024 Dec;181:117731. doi: 10.1016/j.biopha.2024.117731. Epub 2024 Dec 9.
2
Development of dual GPBAR1 agonist and RORγt inverse agonist for the treatment of inflammatory bowel diseases.开发双重 GPBAR1 激动剂和 RORγt 反向激动剂用于治疗炎症性肠病。
Pharmacol Res. 2024 Oct;208:107403. doi: 10.1016/j.phrs.2024.107403. Epub 2024 Sep 10.
3
Therapeutic role of ursodeoxycholic acid in colitis-associated cancer via gut microbiota modulation.
熊去氧胆酸通过调节肠道微生物群在结肠炎相关癌症中的治疗作用。
Mol Ther. 2023 Feb 1;31(2):585-598. doi: 10.1016/j.ymthe.2022.10.014. Epub 2022 Oct 29.
4
Farnesoid X receptor mediates macrophage-intrinsic responses to suppress colitis-induced colon cancer progression.法尼醇 X 受体介导巨噬细胞内在反应抑制结肠炎诱导的结肠癌进展。
JCI Insight. 2024 Jan 23;9(2):e170428. doi: 10.1172/jci.insight.170428.
5
Gut microbiota-derived 12-ketolithocholic acid suppresses the IL-17A secretion from colonic group 3 innate lymphoid cells to prevent the acute exacerbation of ulcerative colitis.肠道微生物群衍生的 12-酮石胆酸抑制结肠固有淋巴细胞 3 群中白细胞介素-17A 的分泌，从而预防溃疡性结肠炎的急性恶化。
Gut Microbes. 2023 Dec;15(2):2290315. doi: 10.1080/19490976.2023.2290315. Epub 2023 Dec 8.
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