肠道菌群代谢物次级胆汁酸调控宿主免疫功能

doi:10.16352/j.issn.1001-6325.2024.06.0887

基础医学与临床 ›› 2024, Vol. 44 ›› Issue (6): 887-891.doi: 10.16352/j.issn.1001-6325.2024.06.0887

肠道菌群代谢物次级胆汁酸调控宿主免疫功能

岳玲玲, 王梓潓, 李小芹, 李利锋, 张万存, 于志丹^*

郑州大学附属儿童医院河南省儿童医院郑州儿童医院郑州市儿童消化疾病重点实验室,河南郑州 450018

收稿日期:2023-09-15 修回日期:2024-01-23 出版日期:2024-06-05 发布日期:2024-05-24
通讯作者: ^*zhidanyu2013@126.com
基金资助:
国家自然科学基金(81903330);河南省科技攻关(202102310071);河南省医学科技攻关(SBGJ202303047)

Regulation of host immune function by gut microbiota-derived secondary bile acids

YUE Lingling, WANG Zihui, LI Xiaoqin, LI Lifeng, ZHANG Wancun, YU Zhidan^*

Zhengzhou Key Laboratory of Children's Digestive Diseases, Henan Children's Hospital Zhengzhou Children's Hospital, Children's Hospital Affiliated to Zhengzhou University, Zhengzhou 450018, China

Received:2023-09-15 Revised:2024-01-23 Online:2024-06-05 Published:2024-05-24
Contact: ^*zhidanyu2013@126.com

摘要/Abstract

摘要： 肠道菌群紊乱破坏宿主免疫系统的平衡。肠道菌群代谢产生许多与宿主相互作用的生物活性分子,典型代表是次级胆汁酸(SBAs)。SBAs通过结合膜受体和核受体,例如武田G蛋白偶联受体5(TGR5)和法尼醇X受体(FXR),参与调控能量代谢和炎性反应相关基因的表达,对维持宿主免疫稳态具有重要意义。

关键词: 肠道菌群, 次级胆汁酸, 免疫调控

Abstract: Disturbances of gut microbiota may affect the balance of the host immune system. The metabolism of gut microbiota produces many bioactive molecules interacting with host, typically secondary bile acids (SBAs). SBAs are involved in regulating the energy metabolism and the expression of inflammatory response-related genes by binding to membrane receptors and nuclear receptors, such as takeda G protein-coupled receptor (TGR5) and farnesol X receptor (FXR), which are essential for maintaining host immune homeostasis.

Key words: gut microbiota, secondary bile acids, immune regulation

中图分类号:

R392.32

岳玲玲, 王梓潓, 李小芹, 李利锋, 张万存, 于志丹. 肠道菌群代谢物次级胆汁酸调控宿主免疫功能[J]. 基础医学与临床, 2024, 44(6): 887-891.

YUE Lingling, WANG Zihui, LI Xiaoqin, LI Lifeng, ZHANG Wancun, YU Zhidan. Regulation of host immune function by gut microbiota-derived secondary bile acids[J]. Basic & Clinical Medicine, 2024, 44(6): 887-891.

参考文献 25

[1]	Wu J, Wang K, Wang X, et al. The role of the gut microbiome and its metabolites in metabolic diseases[J]. Protein Cell, 2021,12:360-373.
[2]	Yang W, Cong Y. Gut microbiota-derived metabolites in the regulation of host immune responses and immune-related inflammatory diseases[J]. Cell Mol Immunol, 2021,18:866-877.
[3]	Funabashi M, Grove TL, Wang M, et al. A metabolic pathway for bile acid dehydroxylation by the gut microbi-ome[J]. Nature, 2020,582:566-570.
[4]	Shi L, Jin L, Huang W. Bile acids, intestinal barrier dysfunction, and related diseases[J]. Cells, 2023,12:1888. doi: 10.3390/cells12141888.
[5]	Hang S, Paik D, Yao L, et al. Bile acid metabolites control T(H)17 and T(reg) cell differentiation[J]. Nature, 2019,576:143-148.
[6]	Campbell C, McKenney PT, Konstantinovsky D, et al. Bacterial metabolism of bile acids promotes generation of peripheral regulatory T cells[J]. Nature, 2020,581:475-479.
[7]	Guo C, Xie S, Chi Z, et al. Bile acids control inflammation and metabolic disorder through inhibition of NLRP3 inflammasome[J]. Immunity, 2016,45:802-816.
[8]	Wang L, Gong Z, Zhang X, et al. Gut microbial bile acid metabolite skews macrophage polarization and contributes to high-fat diet-induced colonic inflammation[J]. Gut Microbes, 2020,12:1-20.
[9]	Lamichhane S, Sen P, Dickens AM, et al. Dysregulation of secondary bile acid metabolism precedes islet autoimmunity and type 1 diabetes[J]. Cell Rep Med, 2022,3:100762. doi: 10.1016/j.xcrm.2022.100762.
[10]	Pathak P, Liu H, Boehme S, et al. Farnesoid X receptor induces Takeda G-protein receptor 5 cross-talk to regulate bile acid synthesis and hepatic metabolism[J]. J Biol Chem, 2017,292:11055-11069.
[11]	Watanabe M, Houten SM, Mataki C, et al. Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation[J]. Nature, 2006,439:484-489.
[12]	Ferrell JM, Chiang J. Understanding bile acid signaling in diabetes: from pathophysiology to therapeutic targets[J]. Diabetes Metab J, 2019,43:257-272.
[13]	Sinha SR, Haileselassie Y, Nguyen LP, et al. Dysbiosis-induced secondary bile acid deficiency promotes intestinal inflammation[J]. Cell Host Microbe, 2020,27:659-670.
[14]	Zeng H, Safratowich BD, Cheng WH, et al. Deoxycholic acid modulates cell-junction gene expression and increases intestinal barrier dysfunction[J]. Molecules, 2022,27:723. doi: 10.3390/molecules27030723.
[15]	Zhao S, Gong Z, Du X, et al. Deoxycholic acid-mediated sphingosine-1-phosphate receptor 2 signaling exacerbates DSS-induced colitis through promoting cathepsin B release[J]. J Immunol Res, 2018,2018:2481418. doi: 10.1155/2018/2481418.
[16]	Ma C, Han M, Heinrich B, et al. Gut microbiome-mediated bile acid metabolism regulates liver cancer via NKT cells[J]. Science, 2018,360:eaan5931. doi: 10.1126/science.aan5931.
[17]	Gillard J, Clerbaux L, Nachit M, et al. Bile acids contribute to the development of non-alcoholic steatohepatitis in mice[J]. JHEP Rep, 2021,4:100387. doi: 10.1016/j.jhepr.2021.100387.
[18]	Hu J, Hong W, Yao KN, et al. Ursodeoxycholic acid ameliorates hepatic lipid metabolism in LO2 cells by regulating the AKT/mTOR/SREBP-1 signaling pathway [J]. World J Gastroenterol, 2019,25:1492-1501.
[19]	Song X, An Y, Chen D, et al. Microbial metabolite deoxycholic acid promotes vasculogenic mimicry formation in intestinal carcinogenesis[J]. Cancer Sci, 2022,113:459-477.
[20]	Farhana L, Nangia-Makker P, Arbit E, et al. Bile acid: a potential inducer of colon cancer stem cells[J]. Stem Cell Res Ther, 2016,7:181. doi: 10.1186/s13287-016-0439-4.
[21]	Gilbert JA, Blaser MJ, Caporaso JG, et al. Current understanding of the human microbiome[J]. Nat Med, 2018,24:392-400.
[22]	von Schwartzenberg RJ, Bisanz JE, Lyalina S, et al. Caloric restriction disrupts the microbiota and colonization resistance[J]. Nature, 2021,595:272-277.
[23]	Yang ZD, Guo YS, Huang JS, et al. Isomaltulose exhibits prebiotic activity, and modulates gut microbiota, the production of short chain fatty acids, and secondary bile acids in rats[J]. Molecules, 2021,26:2464. doi: 10.3390/molecules26092464.
[24]	Song P, Zhang X, Feng W, et al. Biological synthesis of ursodeoxycholic acid[J]. Front Microbiol, 2023,14:1140662. doi: 10.3389/fmicb.2023.1140662.
[25]	Sorrentino G, Perino A, Yildiz E, et al. Bile acids signal via TGR5 to activate intestinal stem cells and epithelial regeneration[J]. Gastroenterology, 2020,159:956-968.

肠道菌群代谢物次级胆汁酸调控宿主免疫功能

Regulation of host immune function by gut microbiota-derived secondary bile acids

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献 25

相关文章 15

编辑推荐

Metrics

本文评价

[1]	何昀, 肖力, 曹娟, 刘志刚, 罗威耀. 奥美拉唑联合不同益生菌调节肠道菌群减轻小儿功能性消化不良[J]. 基础医学与临床, 2024, 44(2): 219-224.
[2]	吕彦函, 余卓颖, 李民. 肠道菌群在神经病理性疼痛中作用的研究进展[J]. 基础医学与临床, 2023, 43(1): 188-191.
[3]	栾格, 王明, 王成硕, 张罗. 干扰素调节因子4(IRF4)在慢性炎性疾病中作用的研究进展[J]. 基础医学与临床, 2022, 42(7): 1119-1123.
[4]	王振花, 李潮生. 饮食作用的肠道菌群-免疫轴与高血压相关性的研究进展[J]. 基础医学与临床, 2022, 42(6): 983-987.
[5]	尹欢欢, 施潇潇, 陈丽萌. 肠-肾轴在新月体肾炎发病机制中的研究进展[J]. 基础医学与临床, 2022, 42(4): 656-660.
[6]	胡贤良, 万燕, 冯霁. 肠道菌群在妊娠期糖尿病发病中作用的研究进展[J]. 基础医学与临床, 2022, 42(3): 516-519.
[7]	李春美, 赵微, 解相宏, 张伟虹, 杨佳卉, 李军, 刘晓军. 青稞酥油饮食对小鼠肠道菌群以及葡聚糖硫酸钠诱导的小鼠结肠炎症状的影响[J]. 基础医学与临床, 2021, 41(2): 203-208.
[8]	王紫涵, 罗金定, 田英入, 奉水东, 凌宏艳. 小胶质细胞引起和促进阿尔茨海默病的研究进展[J]. 基础医学与临床, 2021, 41(2): 277-281.
[9]	牛晓丹, 郭静波, 王惠琳, 迟俊婷, 阮海慧, 陶红霞, 王艳红. 肠道菌群与衰弱关系的研究进展[J]. 基础医学与临床, 2021, 41(1): 108-111.
[10]	邵瑞飞, 杨艳, 郑志榕, 赵世民, 陈国兵. 肠道菌群和“肠-肺”轴在脓毒症中的作用[J]. 基础医学与临床, 2020, 40(8): 1109-1112.
[11]	张静, 王肖枭, 周怡, 王雪, 顾开明, 叶迎春. 肠道菌群与疾病相关性的研究进展[J]. 基础医学与临床, 2020, 40(2): 243-247.
[12]	李曼玉, 尹婕, 马良坤. 长期低剂量抗生素的暴露对孕妇及婴幼儿的影响[J]. 基础医学与临床, 2020, 40(2): 253-256.
[13]	赵军梅, 袁丽萍, 蔡洁, 李文亚, 朱克然, 桂明. 肠易激综合征患儿肠道菌群可促进小鼠肠道酸敏感离子通道蛋白的表达[J]. 基础医学与临床, 2020, 40(2): 173-177.
[14]	王亚楠孟祥辰王春赛尔钱家鸣李景南. 乳果糖增加正常小鼠肠道益生菌群的种类和数量[J]. 基础医学与临床, 2019, 39(6): 786-791.
[15]	金华. 肠道菌群是高血压干预的新靶点[J]. 基础医学与临床, 2018, 38(3): 413-417.