Inflammation-associated depression: From serotonin to kynurenine
Open accessAbstract
In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptophan degrading enzyme indoleamine 2,3-dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms.
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The reciprocal relationship between stress and depression and anxiety is well established.
“The reciprocal relationship between stress and depression and anxiety is well established (Dantzer, 2012;Dantzer, O'Connor, Lawson, & Kelley, 2011;Maes, 2008).”
From The impact of stress on students in secondary school and higher education (2020) · cites this paper as Dantzer, O'Connor, Lawson, & Kelley, 2011
The Human studies section links psychosocial stress to inflammatory activity and reports a correlation between inflammation and depression-like neural activity during bereavement. It does not establish a reciprocal relationship between stress and depression, or address a reciprocal relationship with anxiety. Page numbers were not available in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredIn preclinical models, LPS-induced inflammation increases IDO activity, shifting tryptophan metabolism toward the kynurenine pathway rather than serotonin synthesis.
“In preclinical models, activation of inflammation using LPS increases the activity of IDO thereby allocating more tryptophan metabolism toward the kynurenine pathway rather than serotonin synthesis (Zunszain et al., 2012), ultimately resulting in serotonin deficiency (See Dantzer et al., 2011; Nikkheslat et al., 2018; O’Farrell and Harkin, 2017 for a review of research on the kynurenine pathway).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Dantzer et al., 2011
These metabolites can interact with neurotransmitter systems in the brain, particularly glutamate, and are thought to be involved in the behavioral effects of cytokines.
“These metabolites can then interact with neurotransmitter systems in the brain, particularly glutamate (see Section 3.3), and are thought to be involved in the behavioral effects of cytokines (Dantzer et al., 2011, Haroon et al., 2012).”
From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Dantzer et al., 2011
Inflammatory cytokines activate IDO and KYN pathways in the brain that affect glutamate neurotransmission and may contribute to glutamate dysfunction in depression.
“Inflammatory cytokines activate IDO and KYN pathways in the brain that effect glutamate neurotransmission and may contribute to glutamate dysfunction in depression (McNally et al., 2008, Dantzer et al., 2011, Haroon et al., 2012).”
From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Dantzer et al., 2011
The tryptophan-kynurenine pathway has recently been highlighted in the pathophysiological understanding of MDD beyond the traditional serotonin hypothesis.
“The tryptophan-kynurenine pathway has recently been highlighted in pathophysiological understanding of MDD beyond the traditional”
From Tryptophan-kynurenine and lipid related metabolites as blood biomarkers for first-episode drug-naïve patients with major depressive disorder: An exploratory pilot case-control study (2018) · cites this paper as Dantzer et al., 2011
The study did not measure neurotoxic kynurenine-pathway metabolites such as 3-hydroxykynurenine and quinolinic acid.
“Substances not measured in the present study are neurotoxic kynurenine-pathway metabolites such as 3-hydroxykynurenine and quinolinic acid that have been suggested to be important for further understanding of imbalance of tryptophan-kynurenine pathway in MDD (Dantzer et al., 2011;Halaris et al., 2015;Steiner et al., 2011).”
From Tryptophan-kynurenine and lipid related metabolites as blood biomarkers for first-episode drug-naïve patients with major depressive disorder: An exploratory pilot case-control study (2018) · cites this paper as Dantzer et al., 2011
Both tryptophan-kynurenine metabolites and cholesterol have been suggested to be involved in inflammation.
“Both tryptophan-kynurenine metabolites and cholesterol have been suggested to be involved in inflammation (Dantzer, 2017;Dantzer et al., 2011;Halaris et al., 2015;Maes et al., 2012;Maes et al., 2011b;Myint, 2012;Myint et al., 2012;Parekh et al., 2017).”
From Tryptophan-kynurenine and lipid related metabolites as blood biomarkers for first-episode drug-naïve patients with major depressive disorder: An exploratory pilot case-control study (2018) · cites this paper as Dantzer et al., 2011
Lower kynurenic acid is suggested to lead to lower neuroprotective activity because kynurenic acid antagonizes NMDA and alpha7-nicotinylcholine receptors.
“Lower kynurenic acid, a kynurenine-pathway metabolite, is suggested to lead to lower neuroprotective activity, since kynurenic acid is an antagonist of N-methyl-d-aspartate receptors and alpha7-nicotinylcholine receptors (Dantzer et al., 2011;Maes et al., 2011b;Myint, 2012;Myint et al., 2012;Schwarcz et al., 2012;Schwarcz and Stone, 2017).”
From Tryptophan-kynurenine and lipid related metabolites as blood biomarkers for first-episode drug-naïve patients with major depressive disorder: An exploratory pilot case-control study (2018) · cites this paper as Dantzer et al., 2011
Tryptophan, kynurenine metabolites, and cholesteryl esters are involved not only in major depressive disorder but also in various psychiatric disorders (schizophrenia, bipolar disorder) and physical disorders (inflammatory bowel diseases, infectious diseases, heart diseases).
“Tryptophan, kynurenine metabolites, and CEs have been reported to be involved not only with MDD but also with various psychiatric disorders such as schizophrenia and bipolar disorder and physical disorders such as inflammatory bowel diseases, infectious diseases, and heart diseases (Choi et al., 2017;Dantzer et al., 2011;Halaris, 2013Halaris, , 2017;;Maes et al., 2011b;Martin-Subero et al., 2016;M”
From Tryptophan-kynurenine and lipid related metabolites as blood biomarkers for first-episode drug-naïve patients with major depressive disorder: An exploratory pilot case-control study (2018) · cites this paper as Dantzer et al., 2011
Systemic immune activation has been implicated in the pathophysiology of depression.
“Systemic immune activation has been implicated in the pathophysiology of depression [69].”
From Role of diet and its effects on the gut microbiome in the pathophysiology of mental disorders (2022) · cites this paper as [69]
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- Authors
- Dantzer, R., O’Connor, J. C., Lawson, M. A., & Kelley, K. W.
- Affiliations
- University of Illinois Urbana-Champaign (US)
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Dantzer, Robert
- Venue
- Psychoneuroendocrinology
- Publisher
- Elsevier BV
- Published
- 2011-04
- Volume
- 36
- Issue
- 3
- Pages
- 426-436
- ISSN
- 0306-4530 (ISSN-L)
- PMC
- PMC3053088
- OpenAlex
- W1978830885
- Cited by
- 726
- References
- 91
- Citations by year
- 2026: 34 · 2025: 25 · 2024: 33 · 2023: 31 · 2022: 52 · 2021: 51 · 2020: 56 · 2019: 55 · 2018: 70 · 2017: 45 · 2016: 57 · 2015: 68 · 2014: 44 · 2013: 45 · 2012: 36
- FWCI
- 2.35
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Psychoneuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG029573, R01AG029573)
- National Institute of Mental Health (MH-079829, R01MH079829, MH 71349, R01MH071349, R01MH051569, MH51569)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- kynurenine pathway, serotonin, indoleamine 2,3-dioxygenase, tryptophan metabolism, 3-hydroxykynurenine, quinolinic acid, neuroinflammation, cytokine therapy, animal models of depression, neuroimmune mechanisms, depression pathogenesis
- MeSH terms
- Animals, Depression, Disease Models, Animal, Humans, Inflammation, Kynurenine, Models, Biological, Serotonin, Signal Transduction, Cytokines
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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