Tryptophan Metabolism in Inflammaging: From Biomarker to Therapeutic Target

Sorgdrager, F. J. H., Naude, P. J. W., Kema, I. P., Nollen, E. A. & De Deyn, P. P., 30-Oct-2019, In : Frontiers in Immunology. 10, 8 p., 2565.

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Inflammation aims to restore tissue homeostasis after injury or infection. Age-related decline of tissue homeostasis causes a physiological low-grade chronic inflammatory phenotype known as inflammaging that is involved in many age-related diseases. Activation of tryptophan (Trp) metabolism along the kynurenine (Kyn) pathway prevents hyperinflammation and induces long-term immune tolerance. Systemic Trp and Kyn levels change upon aging and in age-related diseases. Moreover, modulation of Trp metabolism can either aggravate or prevent inflammaging-related diseases. In this review, we discuss how age-related Kyn/Trp activation is necessary to control inflammaging and alters the functioning of other metabolic faiths of Trp including Kyn metabolites, microbiota-derived indoles and nicotinamide adenine dinucleotide (NAD(+)). We explore the potential of the Kyn/Trp ratio as a biomarker of inflammaging and discuss how intervening in Trp metabolism might extend health- and lifespan.

Original languageEnglish
Article number2565
Number of pages8
JournalFrontiers in Immunology
Publication statusPublished - 30-Oct-2019


  • tryptophan, aging, inflammation, kynurenine, inflammaging, tryptophan 2, 3-dioxygenase (TDO), indoleamine 2, 3 dioxygenases (IDO), ARYL-HYDROCARBON RECEPTOR, INDOLEAMINE 2,3-DIOXYGENASE ACTIVITY, KYNURENINE PATHWAY, CARDIOVASCULAR RISK, APOPTOTIC CELLS, OLDER-ADULTS, T-CELLS, ACID, TOLERANCE, INHIBITION

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