The tryptophan metabolic pathway of the microbiome and host cells in health and disease

被引:6
|
作者
Miyamoto, Kentaro [1 ,2 ]
Sujino, Tomohisa [3 ,4 ]
Kanai, Takanori [1 ]
机构
[1] Keio Univ, Sch Med, Dept Internal Med, Div Gastroenterol & Hepatol, Tokyo, Japan
[2] Miyarisan Pharmaceut Co Res Lab, Tokyo, Japan
[3] Keio Univ, Sch Med, Ctr Diag & Therapeut Endoscopy, Tokyo, Japan
[4] Keio Univ, Keio Global Res Inst, Tokyo, Japan
基金
日本科学技术振兴机构;
关键词
brain disease; GPR35; immune cell; kynurenic acid; ARYL-HYDROCARBON RECEPTOR; REGULATORY T-CELLS; GUT MICROBIOTA; KYNURENIC ACID; THERAPEUTIC TARGET; QUINOLINIC ACID; TH17; CELLS; BRAIN; SEROTONIN; MODULATION;
D O I
10.1093/intimm/dxae035
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The intricate and dynamic tryptophan (Trp) metabolic pathway in both the microbiome and host cells highlights its profound implications for health and disease. This pathway involves complex interactions between host cellular and bacteria processes, producing bioactive compounds such as 5-hydroxytryptamine (5-HT) and kynurenine derivatives. Immune responses to Trp metabolites through specific receptors have been explored, highlighting the role of the aryl hydrocarbon receptor in inflammation modulation. Dysregulation of this pathway is implicated in various diseases, such as Alzheimer's and Parkinson's diseases, mood disorders, neuronal diseases, autoimmune diseases such as multiple sclerosis (MS), and cancer. In this article, we describe the impact of the 5-HT, Trp, indole, and Trp metabolites on health and disease. Furthermore, we review the impact of microbiome-derived Trp metabolites that affect immune responses and contribute to maintaining homeostasis, especially in an experimental autoimmune encephalitis model of MS.
引用
收藏
页码:601 / 616
页数:16
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