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Disentangling tryptophan metabolism in inflammatory bowel diseases
  1. Christoph Becker1,
  2. Timon Erik Adolph2
  1. 1Department of Medicine 1, Friedrich-Alexander University of Erlangen-Nuremberg, Erlangen, Bayern, Germany
  2. 2Internal Medicine I, Gastroenterology, Hepatology & Metabolism, Medizinische Universitat Innsbruck, Innsbruck, Austria
  1. Correspondence to Dr Timon Erik Adolph, Internal Medicine I, Medizinische Universitat Innsbruck, Innsbruck 6020, Austria; timon-erik.adolph{at}i-med.ac.at

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The concept that the cellular metabolism of immune and tissue-resident cells controls immune responses in and beyond the gut has emerged over the last decades.1 In the gut mucosa, cell metabolism is shaped by our diet and the commensal microbiota.2 The essential amino acid tryptophan, which is enriched in animal-based protein derived from, for example, egg, red and white meat, fish and milk, is metabolised by the gut microbiota and host cells generating metabolites with immune-modulatory functions. Microbes metabolise tryptophan into indole metabolites generating ligands for aryl hydrocarbon receptor (AhR) signalling at mucosal surfaces of mammals.3 It has been demonstrated that the commensal gut microbiota of mammals controls mucosal T-cell responses by the generation of indoles4 and tryptophan metabolism controls inflammatory cytokine production.5 In the early 2000’s, tryptophan has gained increasing attention for the treatment of inflammatory conditions, partly because experimental autoimmune encephalomyelitis (phenocopying aspects of multiple sclerosis) was ameliorated by treatment with a synthetic tryptophan metabolite in mice.6 Mammalian metabolism of tryptophan in gut epithelium and in mucosal immune cells involves the enzyme indoleamine 2,3-dioxygenase 1 (IDO1), which catalyses the generation of bioactive compounds such as kynurenines.7 Kynurenines serve a wide range of physiological functions, maintaining health or promoting disease, …

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Footnotes

  • Contributors CB and TEA wrote the commentary.

  • Funding CB is supported by the DFG projects SFB1181 (C05), TRR241 (A03) and BE3686/9, and by the Interdisciplinary Center for Clinical Research (IZKF A76). TA is grateful for funding from the European Union (ERC-STG grant agreement No. 101039320) and the Austrian Science Fund (FWF P33070).

  • Disclaimer Views and opinions expressed are, however, those of the authors only and do not necessarily reflect those of the European Union or the European Research Council Executive Agency. Neither the European Union nor the granting authority can be held responsible for them.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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