Microbial tryptophan catabolites in health and disease

Research output: Contribution to journal › Review › peer-review

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Microbial tryptophan catabolites in health and disease. / Roager, Henrik Munch; Licht, Tine Rask.

In: Nature Communications, Vol. 9, 3294, 2018.

Research output: Contribution to journal › Review › peer-review

Harvard

Roager, HM & Licht, TR 2018, 'Microbial tryptophan catabolites in health and disease', Nature Communications, vol. 9, 3294. https://doi.org/10.1038/s41467-018-05470-4

APA

Roager, H. M., & Licht, T. R. (2018). Microbial tryptophan catabolites in health and disease. Nature Communications, 9, [3294]. https://doi.org/10.1038/s41467-018-05470-4

Vancouver

Roager HM, Licht TR. Microbial tryptophan catabolites in health and disease. Nature Communications. 2018;9. 3294. https://doi.org/10.1038/s41467-018-05470-4

Author

Roager, Henrik Munch ; Licht, Tine Rask. / Microbial tryptophan catabolites in health and disease. In: Nature Communications. 2018 ; Vol. 9.

Bibtex

@article{a313e63354db491199cb512600a3a319,
title = "Microbial tryptophan catabolites in health and disease",
abstract = "Accumulating evidence implicates metabolites produced by gut microbes as crucial mediators of diet-induced host-microbial cross-talk. Here, we review emerging data suggesting that microbial tryptophan catabolites resulting from proteolysis are influencing host health. These metabolites are suggested to activate the immune system through binding to the aryl hydrocarbon receptor (AHR), enhance the intestinal epithelial barrier, stimulate gastrointestinal motility, as well as secretion of gut hormones, exert anti-inflammatory, antioxidative or toxic effects in systemic circulation, and putatively modulate gut microbial composition. Tryptophan catabolites thus affect various physiological processes and may contribute to intestinal and systemic homeostasis in health and disease.",
author = "Roager, {Henrik Munch} and Licht, {Tine Rask}",
note = "CURIS 2018 NEXS 300",
year = "2018",
doi = "10.1038/s41467-018-05470-4",
language = "English",
volume = "9",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Microbial tryptophan catabolites in health and disease

AU - Roager, Henrik Munch

AU - Licht, Tine Rask

N1 - CURIS 2018 NEXS 300

PY - 2018

Y1 - 2018

N2 - Accumulating evidence implicates metabolites produced by gut microbes as crucial mediators of diet-induced host-microbial cross-talk. Here, we review emerging data suggesting that microbial tryptophan catabolites resulting from proteolysis are influencing host health. These metabolites are suggested to activate the immune system through binding to the aryl hydrocarbon receptor (AHR), enhance the intestinal epithelial barrier, stimulate gastrointestinal motility, as well as secretion of gut hormones, exert anti-inflammatory, antioxidative or toxic effects in systemic circulation, and putatively modulate gut microbial composition. Tryptophan catabolites thus affect various physiological processes and may contribute to intestinal and systemic homeostasis in health and disease.

AB - Accumulating evidence implicates metabolites produced by gut microbes as crucial mediators of diet-induced host-microbial cross-talk. Here, we review emerging data suggesting that microbial tryptophan catabolites resulting from proteolysis are influencing host health. These metabolites are suggested to activate the immune system through binding to the aryl hydrocarbon receptor (AHR), enhance the intestinal epithelial barrier, stimulate gastrointestinal motility, as well as secretion of gut hormones, exert anti-inflammatory, antioxidative or toxic effects in systemic circulation, and putatively modulate gut microbial composition. Tryptophan catabolites thus affect various physiological processes and may contribute to intestinal and systemic homeostasis in health and disease.

U2 - 10.1038/s41467-018-05470-4

DO - 10.1038/s41467-018-05470-4

M3 - Review

C2 - 30120222

VL - 9

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 3294

ER -

ID: 201149189