Evidence for sustained elevation of IL-6 in the CNS as a key contributor of depressive-like phenotypes
Open accessAbstract
There is compelling clinical literature implicating a role for cytokines in the pathophysiology of major depressive disorder (MDD). Interleukin-6 (IL-6) and interleukin-1β (IL-1β) are pleiotropic inflammatory cytokines that have been reported to be elevated in patients with MDD. The present studies were undertaken to investigate the relationship between IL-6 and IL-1β in animal models of depressive-like behavior. Analysis of brain tissue homogenates in the cortex of rats subjected to chronic stress paradigms revealed elevated levels of IL-6 protein in the absence of elevations in IL-1β. Central administration of recombinant mouse IL-6 produced depressive-like phenotypes in mice, which were not accompanied by IL-1β-induced increases in the brain tissue or IL-1β-related sickness behavior typical of a general central nervous system inflammatory response. Systemic administration of fluoxetine in the presence of centrally administered IL-6 failed to produce the expected antidepressant-like response in mice relative to sham-infused controls. Further, administration of fluoxetine to mice with endogenous overexpression of brain IL-6 (MRL/MpJ-Fas(LPR/LPR) (LPR mice)) failed to produce the expected antidepressant-like effect relative to fluoxetine-treated control mice (MRL/MpJ(+/+)). Interestingly, blockade of IL-6 trans-signaling by coadministration of a gp130/Fc monomer or an anti-mouse IL-6 antibody with IL-6 prevented the IL-6-induced increases in immobility time as well as attenuated IL-6-induced increases of protein in the cortex. Taken together, these data indicate that elevations in IL-6 may have a pathophysiological role underlying depression and more specifically resistance to current classes of antidepressant medications and suggest that modulation of the IL-6 signaling pathway may have therapeutic potential for treatment-resistant depression.
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The literature describing the effects of standard antidepressants on systemic inflammation is highly mixed.
“Indeed, the literature describing the effects of standard antidepressants on systemic inflammation is highly mixed.”
From Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress (2014) · cites this paper as [31]
The Introduction (page unavailable) reports that plasma IL-6 normalizes after successful antidepressant treatment but remains elevated in patients who do not respond. That supports differing outcomes by treatment response, but the paper does not characterize the literature on standard antidepressants and systemic inflammation broadly as highly mixed. (LLM, conf=0.78)
Experimental — accuracy not yet measuredSome studies have demonstrated that antidepressants decrease inflammatory cytokines, others report either no effect or even increased levels.
“Although some studies have demonstrated that antidepressants decrease inflammatory cytokines (38, 39), others report either no effect (31, 40, 41) or even increased levels (42, 43).”
From Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress (2014) · cites this paper as [31]
The Introduction (page unavailable) reports normalization of elevated IL-6 after successful antidepressant treatment and persistently elevated IL-6 in patients who do not respond. The Results (page unavailable) also report that fluoxetine only partially attenuated experimentally elevated brain IL-6 in mice. These passages support decreases in some circumstances and persistent elevation in others, but they do not report antidepressants increasing inflammatory cytokine levels. (LLM, conf=0.87)
Experimental — accuracy not yet measuredChronic stress and overexpression of central IL-6 trigger depressive-like behavior in rats, an effect unaltered by SSRI but prevented by IL-6 antibodies.
“For example, chronic stress and overexpression of central IL-6 triggered depressive-like behavior in rats – an effect unaltered by SSRI, but prevented by treatment with IL-6 antibodies [18].”
From Interleukin-6 Induced by Social Stress Promotes a Unique Transcriptional Signature in the Monocytes That Facilitate Anxiety (2019) · cites this paper as [18]
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- Authors
- Sukoff Rizzo, S. J., Neal, S. J., Hughes, Z. A., Beyna, M., Rosenzweig-Lipson, S., Moss, S. J., & Brandon, N. J.
- Affiliations
- Pfizer (United States) (US)
- Tufts University (US)
- Venue
- Translational Psychiatry
- Published
- 2012-12-04
- Volume
- 2
- Issue
- 12
- Pages
- e199-e199
- ISSN
- 2158-3188 (ISSN-L)
- PMC
- PMC3565187
- OpenAlex
- W1975588273
- Cited by
- 241
- References
- 66
- Citations by year
- 2026: 10 · 2025: 11 · 2024: 11 · 2023: 16 · 2022: 14 · 2021: 20 · 2020: 21 · 2019: 26 · 2018: 17 · 2017: 19 · 2016: 20 · 2015: 22 · 2014: 28 · 2013: 6
- FWCI
- 5.52
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-nd
- www.springer.com/tdm (unspecified)
- Locations
- Translational Psychiatry (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS051195, R01NS081986)
- 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
- interleukin-6, IL-1β, major depressive disorder, depression-like behavior, chronic stress, neuroinflammation, antidepressant resistance, IL-6 trans-signaling, anti-IL-6 antibody, lpr mice, sickness behavior, brain cytokines
- MeSH terms
- Analysis of Variance, Animals, Central Nervous System, Depression, Disease Models, Animal, Fluoxetine, Mice, Inbred Strains, Phenotype, Stress, Physiological, Interleukin-6, Rats, Sprague-Dawley, Cytokine Receptor gp130, Mice, Rats, Interleukin-1beta, Depressive Disorder, Treatment-Resistant
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