Effects of antidepressants on the production of cytokines
Open accessAbstract
There is now evidence that major depression is associated with an up-regulation of the inflammatory response system (IRS). One of the major factors in this IRS activation is the hyperproduction of pro-inflammatory cytokines. Recently, a number of studies examined whether there is a causative role of these inflammatory mediators in the aetiology of major depression. Studies with animal models and cytokine immune therapy in humans suggest that pro-inflammatory cytokines induce depressive symptomatology. Moreover, these depressive symptoms can be effectively reversed by antidepressant treatment. Thus, it may be suggested that antidepressants suppress pro-inflammatory cytokine production and/or action, resulting in improvement of depressive symptoms. The influence of antidepressants on cytokine production has been examined in culture systems in vitro, and in animal models of depression - in which cytokine production is induced by endotoxin administration. Results suggest that antidepressants of several classes decrease the production of pro-inflammatory cytokines such as interferon-gamma and tumour necrosis factor-alpha, and increase that of interleukin-10, an anti-inflammatory cytokine. Further, the effect of antidepressive treatment on cytokine secretion and on plasma levels of cytokines in depressed patients has been studied. Unfortunately, different approaches to examine cytokine production and different techniques to measure cytokines in plasma are used in these studies. Despite this, current data indicate a normalization of cytokine plasma levels and cytokine production after antidepressant treatment. It is clear, however, that more research is warranted and we strongly argue the need for higher standardization in the methodology used to examine the cytokine network in depressed patients.
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Antidepressants exhibit the capacity to inhibit cytokine production both in vitro and in vivo.
“data also indicate that antidepressants exhibit the capacity to inhibit cytokine production both in vitro and in vivo.105”
From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [105]
Both TCAs and SSRIs normalize serum levels of pro-inflammatory cytokines in patients with MDD.
“earlier studies have demonstrated that both TCA and selective serotonin reuptake inhibitors (SSRIs) normalize the serum levels of pro-inflammatory cytokines in patients with MDD [146,147,148]”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [146]
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A detailed examination of cytokine abnormalities in Major Depressive Disorder
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A psychoneuroimmunological review on cytokines involved in antidepressant treatment response
Janssen, D. G. A., Caniato, R. N., Verster, J. C., & Baune, B. T. (2010) · Human Psychopharmacology Clinical and Experimental · doi:10.1002/hup.1103 · Cited by 240 · see citing works
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Inflammation-Associated Co-morbidity Between Depression and Cardiovascular Disease
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Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanisms
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Antidepressant therapies inhibit inflammation and microglial M1-polarization
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Th2 Cytokine Response in Major Depressive Disorder Patients before Treatment
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A critical review of human endotoxin administration as an experimental paradigm of depression.
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Cytokine-induced depression during IFN-α treatment: The role of IL-6 and sleep quality
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Inflammation-induced depression: Its pathophysiology and therapeutic implications
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P2X7 Receptor Signaling in Stress and Depression
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Posttraumatic stress disorder: does the gut microbiome hold the key?
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Regulatory T cells increased while IL-1β decreased during antidepressant therapy
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Imipramine attenuates neuroinflammatory signaling and reverses stress-induced social avoidance
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Interleukin-10: A Key Cytokine in Depression?
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Peripheral Inflammatory Parameters in Late-Life Depression: A Systematic Review
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Self-citationParoxetine suppresses recombinant human P2X7 responses
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Inflammation Through a Psychoneuroimmunological Lens
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Niemegeers, P., de Boer, P., Schuermans, J., Dumont, G. J. H., Coppens, V., Spittaels, K., Claes, S., Sabbe, B. G. C., & Morrens, M. (2019) · Journal of Affective Disorders · doi:10.1016/j.jad.2018.11.020 · Cited by 12 · see citing works
- Authors
- Kenis, G., & Maes, M.
- Affiliations
- Maastricht University (NL)
- ORCID
- Maes, Michael
- Venue
- The International Journal of Neuropsychopharmacology
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-12
- Volume
- 5
- Issue
- 4
- Pages
- 401-412
- ISSN
- 1461-1457 (ISSN-L)
- 1469-5111
- OpenAlex
- W2054492621
- Cited by
- 370
- References
- 78
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 7 · 2023: 12 · 2022: 12 · 2021: 17 · 2020: 10 · 2019: 16 · 2018: 20 · 2017: 25 · 2016: 20 · 2015: 24 · 2014: 17 · 2013: 19 · 2012: 22
- FWCI
- 0.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The International Journal of Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- antidepressants, inflammatory cytokines, major depressive disorder, interferon-gamma, TNF-α, IL-10, endotoxin, animal models of depression, method standardization
- MeSH terms
- Animals, Antidepressive Agents, Brain Chemistry, Depressive Disorder, Humans, Cytokines, In Vitro Techniques
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