Cytokine-induced sickness behaviour: a neuroimmune response to activation of innate immunity
Abstract
Sickness refers to a coordinated set of subjective, behavioural and physiological changes that develop in sick individuals during the course of an infection. These changes are due to the effects of interleukin-1 (IL-1) and other proinflammatory cytokines on brain cellular targets. Sickness behaviour is mediated by proinflammatory cytokines that are temporarily expressed in the brain during infection. These centrally produced cytokines are the same as those expressed by innate immune cells and they act on brain receptors that are identical to those characterized on immune cells. Primary afferent nerves represent the main communication pathway between peripheral and central cytokines. Proinflammatory cytokines modulate learning and memory processes. The expression and action of proinflammatory cytokines in the brain in response to peripheral cytokines are regulated by various molecular intermediates including anti-inflammatory cytokines such as interleukin-10 (IL-10) and the IL-1 receptor antagonist (IL-1ra), growth factors such as insulin-like growth factor-1 (IGF-1), hormones such as glucocorticoids and neuropeptides such as vasopressin and alpha-melanotropin.
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Other studies have failed to find significant group-wise changes in sex hormones in ME/CFS.
“other studies have failed to find significant group-wise changes in sex hormones in ME/CFS54,55”
From Leveraging Prior Knowledge of Endocrine Immune Regulation in the Therapeutically-relevant Phenotyping of Women with Chronic Fatigue Syndrome (2019) · cites this paper as [55]
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Neuroinflammation and comorbidity of pain and depression
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Self-citationSex Differences in Vulnerability and Resilience to Stress Across the Life Span
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Depression, inflammation, and pain in patients with rheumatoid arthritis.
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Biochemical Regulation of Sleep and Sleep Biomarkers
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“A potential role for IL-6 in pathogenesis of depression, psychosis and other major mental disorders is supported by experimental and clinical studies (Dantzer, 2004; Dantzer et al., 2008; Khandaker and Dantzer, 2016; Miller et al., 2009; Raison et al., 2006).”
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- Authors
- Dantzer, R.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Dantzer, Robert
- ORCID
- Dantzer, Robert
- Venue
- European Journal of Pharmacology
- Publisher
- Elsevier BV
- Published
- 2004-10
- Volume
- 500
- Issue
- 1-3
- Pages
- 399-411
- ISSN
- 0014-2999 (ISSN-L)
- OpenAlex
- W2061931936
- Cited by
- 743
- References
- 109
- Citations by year
- 2026: 15 · 2025: 18 · 2024: 28 · 2023: 23 · 2022: 33 · 2021: 47 · 2020: 43 · 2019: 32 · 2018: 32 · 2017: 28 · 2016: 39 · 2015: 31 · 2014: 39 · 2013: 35 · 2012: 43
- FWCI
- 2.12
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- sickness behavior, inflammatory cytokines, interleukin-1, neuroimmune interactions, innate immunity, infection, learning and memory, IL-10, interleukin-1 receptor antagonist, insulin-like growth factor I, glucocorticoids, vasopressin, alpha-melanotropin, cytokine receptors
- MeSH terms
- Animals, Brain, Humans, Immunity, Innate, Infections, Sick Role, Neuroimmunomodulation, Cytokines
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