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World J Gastrointest Pharmacol Ther. Feb 6, 2017; 8(1): 7-9
Published online Feb 6, 2017. doi: 10.4292/wjgpt.v8.i1.7
Tryptophan: A gut microbiota-derived metabolites regulating inflammation
Lucie Etienne-Mesmin, Benoit Chassaing, Andrew T Gewirtz
Lucie Etienne-Mesmin, Benoit Chassaing, Andrew T Gewirtz, Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303, United States
Author contributions: Etienne-Mesmin L wrote the manuscript; Chassaing B and Gewirtz AT critically revised the manuscript.
Supported by National Institutes of Health (NIH), Nos. DK099071 and DK083890; the Career Development Award from the Crohn’s and Colitis Foundation of America (CCFA).
Conflict-of-interest statement: No potential conflicts of interest relevant to this article were reported.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Lucie Etienne-Mesmin, PhD, Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, 100 Piedmont Ave SE, Atlanta, GA 30303, United States.
Telephone: +1-404-4133589 Fax: +1-404-4133580
Received: August 12, 2016
Peer-review started: August 12, 2016
First decision: September 16, 2016
Revised: September 22, 2016
Accepted: October 22, 2016
Article in press: October 24, 2016
Published online: February 6, 2017

Inflammatory bowel diseases (IBD), which comprise Crohn’s disease and ulcerative colitis, are chronic intestinal disorders with an increased prevalence and incidence over the last decade in many different regions over the world. The etiology of IBD is still not well defined, but evidence suggest that it results from perturbation of the homeostasis between the intestinal microbiota and the mucosal immune system, with the involvement of both genetic and environmental factors. Genome wide association studies, which involve large-scale genome-wide screening of potential polymorphism, have identified several mutations associated with IBD. Among them, Card9, a gene encoding an adapter molecule involved in innate immune response to fungi (via type C-lectin sensing) through the activation of IL-22 signaling pathway, has been identified as one IBD susceptible genes. Dietary compounds, which represent a source of energy and metabolites for gut bacteria, are also appreciated to be important actors in the etiology of IBD, for example by altering gut microbiota composition and by regulating the generation of short chain fatty acids. A noteworthy study published in the June 2016 issue of Nature Medicine by Lamas and colleagues investigates the interaction between Card9 and the gut microbiota in the generation of the microbiota-derived tryptophan metabolite. This study highlights the role of tryptophan in dampening intestinal inflammation in susceptible hosts.

Keywords: Intestinal inflammation, Tryptophan, Microbiota

Core tip: A noteworthy article published in Nature Medicine by Lamas and colleagues highlights the role of tryptophan, a microbiota-derived metabolite, in reducing inflammation in the gut. This commentary puts in perspective the main results from this study.