Journal
PSYCHONEUROENDOCRINOLOGY
Volume 71, Issue -, Pages 189-196Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.psyneuen.2016.04.024
Keywords
Plasma; CRP; IL-6; sIL-1RII; Kynurenine pathway; Aggression
Categories
Funding
- National Institute of Mental Health [RO1 MH60836, RO1 MH63262, RO1 MH66984, RO1 MH80108, RO1 MH104622]
- Swedish Medical Research Council
- Swedish Brain Foundation
- Petrus och Auguista Hedlunds Stiftlse
- Project Pilot Grant from University of Colorado Denver
- Azevan Pharmaceuticals, Inc.
- Astra Zenica
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Inflammatory proteins are thought to be causally involved in the generation of aggression, possibly due to direct effects of cytokines in the central nervous system and/or by generation of inflammatory metabolites along the tryptophan-kynurenine (TRP/KYN) pathway, including KYN and its active metabolites kynurenic acid (KA), quinolinic acid (QA), and picolinic acid (PA). We examined plasma levels of TRP, KYN, KA, QA, and PA in 172 medication-free, medically healthy, human subjects to determine if plasma levels of these substances are altered as a function of trait aggression, and if they correlate with current plasma levels of inflammatory markers. Plasma levels of C-reactive protein (CRP), interleukin-6 (IL-6), and soluble interleukin-1 receptor-II (sIL-1RII) protein were also available in these subjects. We found normal levels of TRP but reduced plasma levels of KYN (by 48%), QA (by 6%), and a QA/KA (by 5%) ratio in subjects with Intermittent Explosive Disorder (IED) compared to healthy controls and psychiatric controls. Moreover, the metabolites were not associated with any of the inflammatory markers studied. These data do not support the hypothesis that elevated levels of KYN metabolites would be present in plasma of subjects with IED, and associated with plasma inflammation. However, our data do point to a dysregulation of the KYN pathway metabolites in these subjects. Further work will be necessary to replicate these findings and to understand their role in inflammation and aggression in these subjects. (C) 2016 Elsevier Ltd. All rights reserved.
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