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      Microbial tryptophan catabolites in health and disease

      review-article
      Author(s): 1 , 2 , , 2 ,
      Publication date (Electronic):
      Journal: Nature Communications
      Publisher: Nature Publishing Group UK

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          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, anti-oxidative 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.

          Abstract

          Gut microbial metabolites are known to impact many physiological processes of the host and play a critical role in immune-homeostasis. Here the authors review our current understanding and appreciation of the importance of microbially derived tryptophan catabolites during both health and disease.

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          The maternal microbiota drives early postnatal innate immune development.

          Mercedes Gomez de Agüero, Stephanie C Ganal-Vonarburg, Tobias Fuhrer … (2016)
          Postnatal colonization of the body with microbes is assumed to be the main stimulus to postnatal immune development. By transiently colonizing pregnant female mice, we show that the maternal microbiota shapes the immune system of the offspring. Gestational colonization increases intestinal group 3 innate lymphoid cells and F4/80(+)CD11c(+) mononuclear cells in the pups. Maternal colonization reprograms intestinal transcriptional profiles of the offspring, including increased expression of genes encoding epithelial antibacterial peptides and metabolism of microbial molecules. Some of these effects are dependent on maternal antibodies that potentially retain microbial molecules and transmit them to the offspring during pregnancy and in milk. Pups born to mothers transiently colonized in pregnancy are better able to avoid inflammatory responses to microbial molecules and penetration of intestinal microbes.
          Article 0 comments Cited 509 times – based on 0 reviews     Review now
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            Linking the Human Gut Microbiome to Inflammatory Cytokine Production Capacity.

            Melanie Schirmer, Sanne Smeekens, Hera Vlamakis … (2016)
            Gut microbial dysbioses are linked to aberrant immune responses, which are often accompanied by abnormal production of inflammatory cytokines. As part of the Human Functional Genomics Project (HFGP), we investigate how differences in composition and function of gut microbial communities may contribute to inter-individual variation in cytokine responses to microbial stimulations in healthy humans. We observe microbiome-cytokine interaction patterns that are stimulus specific, cytokine specific, and cytokine and stimulus specific. Validation of two predicted host-microbial interactions reveal that TNFα and IFNγ production are associated with specific microbial metabolic pathways: palmitoleic acid metabolism and tryptophan degradation to tryptophol. Besides providing a resource of predicted microbially derived mediators that influence immune phenotypes in response to common microorganisms, these data can help to define principles for understanding disease susceptibility. The three HFGP studies presented in this issue lay the groundwork for further studies aimed at understanding the interplay between microbial, genetic, and environmental factors in the regulation of the immune response in humans. PAPERCLIP.
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              Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4.

              Madhukumar Venkatesh, Subhajit Mukherjee, Hongwei Wang … (2014)
              Intestinal microbial metabolites are conjectured to affect mucosal integrity through an incompletely characterized mechanism. Here we showed that microbial-specific indoles regulated intestinal barrier function through the xenobiotic sensor, pregnane X receptor (PXR). Indole 3-propionic acid (IPA), in the context of indole, is a ligand for PXR in vivo, and IPA downregulated enterocyte TNF-α while it upregulated junctional protein-coding mRNAs. PXR-deficient (Nr1i2(-/-)) mice showed a distinctly "leaky" gut physiology coupled with upregulation of the Toll-like receptor (TLR) signaling pathway. These defects in the epithelial barrier were corrected in Nr1i2(-/-)Tlr4(-/-) mice. Our results demonstrate that a direct chemical communication between the intestinal symbionts and PXR regulates mucosal integrity through a pathway that involves luminal sensing and signaling by TLR4.
              Article 0 comments Cited 388 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Henrik M. Roager: hero@nexs.ku.dk
                Tine R. Licht:
                ORCID: http://orcid.org/0000-0002-6399-9574
                trli@food.dtu.dk
                Journal
                Journal ID (nlm-ta): Nat Commun
                Journal ID (iso-abbrev): Nat Commun
                Title: Nature Communications
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-1723
                Publication date (Electronic): 17 August 2018
                Publication date PMC-release: 17 August 2018
                Publication date Collection: 2018
                Volume: 9
                Electronic Location Identifier: 3294
                Affiliations
                [1 ]ISNI 0000 0001 0674 042X, GRID grid.5254.6, Department of Nutrition, Exercise and Sports, Faculty of Science, , University of Copenhagen, ; DK-1958 Frederiksberg, Denmark
                [2 ]ISNI 0000 0001 2181 8870, GRID grid.5170.3, National Food Institute, , Technical University of Denmark, ; DK-2800 Kgs Lyngby, Denmark
                Author information
                http://orcid.org/0000-0002-6399-9574
                Article
                Publisher ID: 5470
                DOI: 10.1038/s41467-018-05470-4
                PMC ID: 6098093
                PubMed ID: 30120222
                SO-VID: efa54b75-a2f2-443a-b584-5f5384a08111
                Copyright © © The Author(s) 2018
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 23 February 2018
                Date accepted : 3 July 2018
                Funding
                Funded by: This work was supported by the Innovation Fund Denmark (grant no. 11-116163/0603-00487B; Center for Gut, Grain and Greens).
                Categories
                Subject: Review Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Uncategorized
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