Treatment of cytokine-induced depression
Abstract
A high proportion of cancer and hepatitis C patients who receive cytokine immunotherapy develop symptoms of depression that are indistinguishable from those found in major depressive disorders. These symptoms are alleviated by anti-depressant treatment. Moreover, preventive treatment with anti-depressants, in particular selective serotonin reuptake inhibitors (SSRIs) attenuates IFN-alpha-associated symptoms of depression, anxiety, and neurotoxicity. The intermediate mechanisms of these effects are still unclear. Studies suggest that the state of depression is associated with an increase in plasma levels of various cytokines and soluble cytokine receptors. Furthermore, anti-depressants have been shown to shift the cytokine network towards a decreased production of pro-inflammatory cytokines and an increased production of anti-inflammatory cytokines. Other studies suggest that anti-depressants can also modify immune reactivity by acting on neural structures involved in neuroimmunomodulation. It is possible that anti-depressants could help to normalize the serotoninergic neurotransmission that is likely disrupted during immunotherapy due to the potent effects of cytokines on the metabolism of the amino acid precursor tryptophan. Further work is needed to optimize strategies for preventing neuropsychiatric side effects of cytokine immunotherapy, to clarify the mechanisms involved in the alleviating effects of anti-depressants on cytokine-induced depression, as well as to assess the possible consequences of anti-depressant therapy on the efficacy of immunotherapy on the disease process.
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Inflammatory interventions can lead to symptoms of depression and anxiety, such as in patients receiving interferon alpha treatment.
“Additional evidence contributing to neuroimmune theories of depression and anxiety arise from observations that inflammatory interventions can lead to symptoms of these disorders, such as in the case of patients receiving interferon (IFN) alpha treatment [64].”
From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [64]
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- Authors
- Capuron, L., Hauser, P., Hinze-Selch, D., Miller, A. H., & Neveu, P. J.
- Affiliations
- Emory University (US)
- Université de Bordeaux (FR)
- Corresponding author
- Neveu, Pierre J
- ORCID
- Capuron, Lucile
- Venue
- Brain Behavior and Immunity
- Publisher
- Elsevier BV
- Published
- 2002-10
- Volume
- 16
- Issue
- 5
- Pages
- 575-580
- ISSN
- 0889-1591 (ISSN-L)
- OpenAlex
- W2002423129
- Cited by
- 132
- References
- 30
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 2 · 2023: 4 · 2022: 5 · 2021: 9 · 2020: 6 · 2019: 6 · 2018: 9 · 2017: 7 · 2016: 7 · 2015: 5 · 2014: 4 · 2013: 6 · 2012: 4
- FWCI
- 0.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- 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
- cytokine therapy, antidepressants, selective serotonin reuptake inhibitors, interferon-alpha, cancer patients, hepatitis C, neurotoxicity, anxiety, neuroimmunomodulation, serotonergic neurotransmission, tryptophan metabolism, inflammatory cytokines, anti-inflammatory cytokines, soluble cytokine receptors, neuropsychiatric adverse effects
- MeSH terms
- Antidepressive Agents, Depressive Disorder, Humans, Immunotherapy, Serotonin, Sleep, Tryptophan, Cytokines, Receptors, Cytokine
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