Tryptophan metabolism and immunogenetics in major depression: A role for interferon-gamma gene

Aye Mu Myint*, Brigitta Bondy, Thomas C. Baghai, Daniela Eser, Caroline Nothdurfter, Cornelius Schuele, Peter Zill, Norbert Mueller, Rainer Rupprecht, Markus J. Schwarz

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

53 Citations (Web of Science)


The tryptophan metabolism and immune activation play a role in pathophysiology of major depressive disorders. The pro-inflammatory cytokine interferon-gamma transcriptionally induces the indoleamine 2,3-dioxygenase enzyme that degrades the tryptophan and thus induces serotonin depletion. The polymorphism of certain cytokine genes was reported to be associated with major depression. We investigated the association between interferon-gamma (IFN gamma) gene CA repeat polymorphism, the profile of serotonin and tryptophan pathway metabolites and clinical parameters in 125 depressed patients and 93 healthy controls. Compared to controls, serum tryptophan and 5-hydroxyindoleacetic acid (5HIAA) concentrations in the patients were significantly lower and serum kynurenine concentrations were significantly higher at baseline (p <0.0001). The presence of IFN gamma CA repeat allele 2 homozygous has significant association with higher kynurenine concentrations in controls (F = 4.47, p = 0.038) as well as in patients (F = 3.79, p = 0.045). The existence of interferon-gamma CA repeat allele 2 (homo- or heterozygous) showed significant association with increase of tryptophan breakdown over time during the study period (F = 6.0, p = 0.019). The results indicated the association between IFN gamma CA repeat allele 2, tryptophan metabolism and the effect of medication.
Original languageEnglish
Pages (from-to)128-133
JournalBrain Behavior and Immunity
Publication statusPublished - Jul 2013


  • Affective disorder
  • Kynurenine pathway
  • Interferon-gamma
  • SNP
  • Tryptophan breakdown
  • Genetics

Cite this