Antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) are attenuated by antiinflammatory drugs in mice and humans
Open accessAbstract
Antiinflammatory drugs achieve their therapeutic actions at least in part by regulation of cytokine formation. A “cytokine hypothesis” of depression is supported by the observation that depressed individuals have elevated plasma levels of certain cytokines compared with healthy controls. Here we investigated a possible interaction between antidepressant agents and antiinflammatory agents on antidepressant-induced behaviors and on p11, a biochemical marker of depressive-like states and antidepressant responses. We found that widely used antiinflammatory drugs antagonize both biochemical and behavioral responses to selective serotonin reuptake inhibitors (SSRIs). In contrast to the levels detected in serum, we found that frontal cortical levels of certain cytokines (e.g., TNFα and IFNγ) were increased by serotonergic antidepressants and that these effects were inhibited by antiinflammatory agents. The antagonistic effect of antiinflammatory agents on antidepressant-induced behaviors was confirmed by analysis of a dataset from a large-scale real-world human study, “sequenced treatment alternatives to relieve depression” (STAR*D), underscoring the clinical significance of our findings. Our data indicate that clinicians should carefully balance the therapeutic benefits of antiinflammatory agents versus the potentially negative consequences of antagonizing the therapeutic efficacy of antidepressant agents in patients suffering from depression.
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Anti-inflammatory drugs interfere with the antidepressant effects of SSRIs by disrupting TNF-related increases in p11.
“antiinflammatory drugs have been found to interfere with the antidepressant effects of SSRIs by disrupting TNF-related increases in p11, a small acidic protein that can have strong antidepressant properties”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Warner-Schmidt et al., 2011
The ‘Effects of SSRIs and NSAIDs on Certain Cytokines and p11’ section (page unavailable) reports that NSAIDs blocked SSRI-induced increases in p11 in mice, and that TNFα signaling was necessary for citalopram-induced p11 increases. The Discussion (page unavailable) also reports reduced SSRI responses with anti-inflammatory drug use, but describes TNFα as one of two cytokines that may be involved. The claim states the TNF–p11 mechanism more definitively than the paper does, particularly for the human finding. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe effects of serotonergic antidepressants on behavior are mediated by TNF-related processes.
“the effects of serotonergic antidepressants on behavior are mediated by TNF-related processes”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Warner-Schmidt, Vanover, Chen, Marshall, & Greengard, 2011
In “Effects of Cytokines and p11 on Behavioral Responses” (page unavailable), citalopram’s behavioral effect was absent in TNFR1 knockout mice in the novelty-suppressed feeding test, supporting a role for TNF-related signaling. But its effect in the tail suspension test persisted in those mice, so the source does not establish that TNF-related processes mediate serotonergic antidepressants’ behavioral effects generally. (LLM, conf=0.86)
Experimental — accuracy not yet measuredInflammatory cytokines and the innate immune response have pivotal roles in synaptic plasticity, neurogenesis, long-term potentiation, and possibly antidepressant response.
“Inflammatory cytokines and the innate immune response have pivotal roles in synaptic plasticity, neurogenesis, long-term potentiation (which is a fundamental process in learning and memory) and possibly antidepressant response123,128.”
From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [123]
The Discussion (page not supplied) links IFNγ to neurogenesis and reports evidence that IFNγ and TNFα may contribute to antidepressant-like responses. Our copy does not establish pivotal roles for cytokines or the innate immune response in synaptic plasticity or long-term potentiation, nor does it address the parenthetical claim about learning and memory. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAcetylsalicylic acid (aspirin) improves the effects of SSRIs.
“In addition, acetylsalicylic acid (aspirin) improves the effects of SSRIs[67].”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [67]
Emerging evidence indicates that some anti-inflammatory treatments may antagonize the effects of commonly used antidepressants, including selective serotonin reuptake inhibitors.
“emerging evidence indicates that some anti-inflammatory treatments may antagonize the effects of commonly used antidepressant treatments including selective serotonin reuptake inhibitors.[44]”
From SUICIDAL IDEATION IS ASSOCIATED WITH ELEVATED INFLAMMATION IN PATIENTS WITH MAJOR DEPRESSIVE DISORDER: Research Article: Suicidal Ideation and Inflammation (2013) · cites this paper as [44]
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- Authors
- Warner-Schmidt, J. L., Vanover, K. E., Chen, E. Y., Marshall, J. J., & Greengard, P.
- Affiliations
- Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10065; and
- Intra Cellular Therapies (United States) (US)
- Rockefeller University (US)
- Corresponding author
- Greengard, Paul
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2011-04-25
- Volume
- 108
- Issue
- 22
- Pages
- 9262-9267
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3107316
- OpenAlex
- W2050961629
- Cited by
- 291
- References
- 31
- Citations by year
- 2026: 4 · 2025: 11 · 2024: 12 · 2023: 12 · 2022: 11 · 2021: 14 · 2020: 11 · 2019: 21 · 2018: 31 · 2017: 22 · 2016: 30 · 2015: 24 · 2014: 23 · 2013: 26 · 2012: 31
- FWCI
- 8.07
- Type
- journal article
- Language
- en
- Update notices
- correction (2011-06-15)
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- W. M. Keck Foundation
- Yale University
- Skirball Foundation
- University of Texas Southwestern Medical Center (NCT00021528)
- National Institutes of Health (NCT00021528, n01mh90003-26-0-0, W81XWH, N01MH90003)
- National Institute on Aging (AG09464, P01AG009464)
- National Institute of Mental Health (MH-074866, N01‐MH‐90003, N01 MH090003, P50MH090963, MH090963, P50MH074866, NCT00021528)
- U.S. Army Medical Research Acquisition Activity
- 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
- selective serotonin reuptake inhibitors, depression, cytokines, p11, antidepressant response, TNF-α, interferon-gamma, frontal cortex, STAR*D, drug interactions, antidepressant efficacy
- MeSH terms
- S100 Calcium Binding Protein A10, Animals, Anti-Inflammatory Agents, Anti-Inflammatory Agents, Non-Steroidal, Antidepressive Agents, Depressive Disorder, Drug Interactions, Fluoxetine, Humans, Male, Mice, Inbred C57BL, S100 Proteins, Citalopram, Cytokines, Annexin A2, Selective Serotonin Reuptake Inhibitors, Mice
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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