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Review
. 2021 Mar;41(2):1061-1088.
doi: 10.1002/med.21752. Epub 2020 Nov 10.

Metabolites of microbiota response to tryptophan and intestinal mucosal immunity: A therapeutic target to control intestinal inflammation

Jie Zhang  1   2 , Shengwei Zhu  3 , Ning Ma  1 , Lee J Johnston  4 , Chaodong Wu  5 , Xi Ma  1
Affiliations
Review

Metabolites of microbiota response to tryptophan and intestinal mucosal immunity: A therapeutic target to control intestinal inflammation

Jie Zhang et al. Med Res Rev. 2021 Mar.

Abstract

In a complex, diverse intestinal environment, commensal microbiota metabolizes excessive dietary tryptophan to produce more bioactive metabolites connecting with kinds of diverse process, such as host physiological defense, homeostasis, excessive immune activation and the progression and outcome of different diseases, such as inflammatory bowel disease, irritable bowel syndrome and others. Although commensal microbiota includes bacteria, fungi, and protozoa and all that, they often have the similar metabolites in tryptophan metabolism process via same or different pathways. These metabolites can work as signal to activate the innate immunity of intestinal mucosa and induce the rapid inflammation response. They are critical in reconstruction of lumen homeostasis as well. This review aims to seek the potential function and mechanism of microbiota-derived tryptophan metabolites as targets to regulate and shape intestinal immune function, which mainly focused on two aspects. First, analyze the character of tryptophan metabolism in bacteria, fungi, and protozoa, and assess the functions of their metabolites (including indole and eight other derivatives, serotonin (5-HT) and d-tryptophan) on regulating the integrity of intestinal epithelium and the immunity of the intestinal mucosa. Second, focus on the mediator and pathway for their recognition, transfer and crosstalk between microbiota-derived tryptophan metabolites and intestinal mucosal immunity. Disruption of intestinal homeostasis has been described in different intestinal inflammatory diseases, available data suggest the remarkable potential of tryptophan-derived aryl hydrocarbon receptor agonists, indole derivatives on lumen equilibrium. These metabolites as preventive and therapeutic interventions have potential to promote proinflammatory or anti-inflammatory responses of the gut.

Keywords: intestinal inflammatory diseases; microbes; mucosal immunity; tryptophan metabolites.

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References

REFERENCES

    1. Ma N, Guo P, Zhang J, et al. Nutrients mediate intestinal bacteria-mucosal immune crosstalk. Front Immunol. 2018;9:5.
    1. Rath CM, Dorrestein PC. The bacterial chemical repertoire mediates metabolic exchange within gut microbiomes. Curr Opin Microbiol. 2012;15(2):147-154.
    1. Shibata N, Kunisawa J, Kiyono H. Dietary and microbial metabolites in the regulation of host immunity. Front Microbiol. 2017;8:2171.
    1. Kim CH. Immune regulation by microbiome metabolites. Immunology. 2018;154(2):220-229.
    1. Ma N, Ma X. Dietary amino acids and the gut-microbiome-immune axis: physiological metabolism and therapeutic prospects. Compr Rev Food Sci Food Saf. 2019;18(1):221-242.

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