Effects of inflammation on the kynurenine pathway in schizophrenia—a systematic review
Open accessAbstract
BACKGROUND: In the last decade, there has been growing evidence that an interaction exists between inflammation and the kynurenine pathway in schizophrenia. Additionally, many authors found microglial activation in cases of schizophrenia due to inflammatory mechanisms related mostly to an increase of pro-inflammatory cytokines. In order to gain new insights into the pathophysiology of schizophrenia, it is important to incorporate the latest published evidence concerning inflammatory mechanisms and kynurenine metabolism. This systematic review aims to collect reliable recent findings within the last decade supporting such a theory. METHODS: A structured search of electronic databases was conducted for publications between 2008 and 2018 to identify eligible studies investigating patients with schizophrenia/psychosis and the relationship between inflammation and kynurenine pathway. Applicable studies were systematically scored using the NIH Quality Assessment Tools. Two researchers independently extracted data on diagnosis (psychosis/schizophrenia), inflammation, and kynurenine/tryptophan metabolites. RESULTS: Ten eligible articles were identified where seven studies assessed blood samples and three assessed cerebrospinal fluid in schizophrenic patients. Of these articles: Four investigated the relationship between immunoglobulins and the kynurenine pathway and found correlations between IgA-mediated responses and levels of tryptophan metabolites (i.e., kynurenine pathway).Five examined the correlation between cytokines and kynurenine metabolites where three showed a relationship between elevated IL-6, TNF-α concentrations, and the kynurenine pathway.Only one study discovered correlations between IL-8 and the kynurenine pathway.Two studies showed correlations with lower concentrations of IL-4 and the kynurenine pathway.Moreover, this systematic review did not find a significant correlation between CRP (n = 1 study), IFN-γ (n = 3 studies), and the kynurenine pathway in schizophrenia. INTERPRETATION: These results emphasize how different inflammatory markers can unbalance the tryptophan/kynurenine pathway in schizophrenia. Several tryptophan/kynurenine pathway metabolites are produced which can, in turn, underlie different psychotic and cognitive symptoms via neurotransmission modulation. However, due to heterogeneity and the shortage of eligible articles, they do not robustly converge to the same findings. Hence, we recommend further studies with larger sample sizes to elucidate the possible interactions between the various markers, their blood vs. CSF ratios, and their correlation with schizophrenia symptoms.
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Dysregulation of the kynurenine pathway has been linked to several brain disorders, including depression, schizophrenia, and autism spectrum disorder.
“Dysregulation of the kynurenine pathway has been linked to several brain disorders, including depression (395), schizophrenia (396, 397), and ASD (398).”
From Diet and the Microbiota–Gut–Brain Axis: Sowing the Seeds of Good Mental Health (2021) · cites this paper as [396]
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Schizophrene Störungen: Die Entwicklung immunologischer Krankheits- und Therapiekonzepte
Himmerich, H., Sorge, S., Kirkby, K. C., et al. (2012) · Der Nervenarzt · Cited by 2 · see citing works
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Flagged first, then by citations
Research works printed but not linked: 1
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Diet and the Microbiota–Gut–Brain Axis: Sowing the Seeds of Good Mental Health
Berding, K., Vlckova, K., Marx, W., Schellekens, H., Stanton, C., Clarke, G., Jacka, F., Dinan, T. G., & Cryan, J. F. (2021) · Advances in Nutrition · doi:10.1093/advances/nmaa181 · Cited by 451 · see citing works
The Role of Cytokines in the Pathogenesis of Schizophrenia
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- Authors
- Pedraz-Petrozzi, B., Elyamany, O., Rummel, C., & Mulert, C.
- Affiliations
- Justus-Liebig-Universität Gießen (DE)
- Venue
- Journal of Neuroinflammation
- Published
- 2020-02-15
- Volume
- 17
- Issue
- 1
- Pages
- 56-56
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC7023707
- OpenAlex
- W3012863670
- Cited by
- 119
- References
- 97
- Citations by year
- 2026: 12 · 2025: 18 · 2024: 20 · 2023: 16 · 2022: 23 · 2021: 20 · 2020: 10
- FWCI
- 1.12
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Justus Liebig Universität Gießen
- Deutscher Akademischer Austauschdienst
- Deutsche Forschungsgemeinschaft (SFB 936)
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- schizophrenia, kynurenine pathway, tryptophan metabolism, neuroinflammation, microglial activation, inflammatory cytokines, interleukin-6, TNF-α, interleukin-8, IL-4, immunoglobulin A, C-reactive protein, interferon-gamma, psychosis, cerebrospinal fluid biomarkers, blood biomarkers
- MeSH terms
- Humans, Inflammation, Kynurenine, Psychotic Disorders, Schizophrenia
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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.
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