Gut Microbiota Regulation of Tryptophan Metabolism in Health and Disease
The gut microbiota is a crucial actor in human physiology. Many of these effects are mediated by metabolites that are either produced by the microbes or derived from the transformation of environmental or host molecules. Among the array of metabolites at the interface between these microorganisms an...
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Published in | Cell host & microbe Vol. 23; no. 6; pp. 716 - 724 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
13.06.2018
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Subjects | |
Online Access | Get full text |
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Summary: | The gut microbiota is a crucial actor in human physiology. Many of these effects are mediated by metabolites that are either produced by the microbes or derived from the transformation of environmental or host molecules. Among the array of metabolites at the interface between these microorganisms and the host is the essential aromatic amino acid tryptophan (Trp). In the gut, the three major Trp metabolism pathways leading to serotonin (5-hydroxytryptamine), kynurenine (Kyn), and indole derivatives are under the direct or indirect control of the microbiota. In this review, we gather the most recent advances concerning the central role of Trp metabolism in microbiota-host crosstalk in health and disease. Deciphering the complex equilibrium between these pathways will facilitate a better understanding of the pathogenesis of human diseases and open therapeutic opportunities.
Many metabolites are involved in host-microbiota interactions. Agus et al. review recent advances concerning the central role of tryptophan metabolism in microbiota-host crosstalk in health and disease. This review examines the direct effect of the gut microbiota in producing tryptophan-derived bioactive molecules and its indirect control of host tryptophan metabolism. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1931-3128 1934-6069 |
DOI: | 10.1016/j.chom.2018.05.003 |