Citalopram reduces endotoxin-induced fatigue
Open accessAbstract
Increased levels of inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin-6 (IL-6) may play a role in depression. Mild depressive-like symptoms can be induced in humans through activation of the innate immune system with endotoxin. Whether preventive treatment with antidepressants can reduce endotoxin-induced symptoms has never been tested. In a double-blind, randomized, placebo-controlled, cross-over study, we administered intravenous low-dose endotoxin (0.8 ng/kg) or placebo to 11 healthy subjects who had received oral pre-treatment with citalopram (10 mg twice a day) or placebo for 5 days. The Montgomery-Åsberg Depression Rating Scale, the State and Trait Anxiety Inventory, and a visual analog scale were used to measure depressive and anxiety symptoms and social anhedonia. Serum levels of TNF and IL-6 were measured with immunoassays. Compared to placebo, endotoxin administration increased serum levels of TNF and IL-6, and caused mild depressive-like symptoms, in particular lassitude and social anhedonia. While citalopram pre-treatment had no effect on the innate immune response to endotoxin, it reduced the endotoxin-induced MADRS total score by 50%, with a moderate effect size (Cohen's d=0.5). Most of the MADRS total score was due to the lassitude item, and citalopram pre-treatment specifically reduced endotoxin-induced lassitude with a large effect size (Cohen's d=0.9). These results suggest that subchronic pre-treatment with the serotonin-reuptake inhibitor citalopram blunts mood symptoms induced by acute immune system activation with endotoxin without inhibiting the peripheral immune response.
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Increases in depressive symptoms following endotoxin administration are associated with changes in levels of IL-6 and TNFα in peripheral blood.
“increases in depressive symptoms following endotoxin administration have been associated with changes in levels of the proinflammatory cytokines IL-6 and TNFα in peripheral blood”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Hannestad, DellaGioia, Ortiz, Pittman, & Bhagwagar, 2011
The Introduction and Results §§3.1–3.2 report that endotoxin increased serum IL-6 and TNF alongside depressive-symptom scores. But Results §3.2 explicitly reports no correlation between either cytokine level and MADRS total or lassitude scores, so the paper supports their concurrent increases, not a direct association between the measured changes. (LLM, conf=0.85)
Experimental — accuracy not yet measuredEffects of endotoxin-induced increases in depressive symptoms can be blunted or abated with antidepressant medications.
“the effects of endotoxin-induced increases in depressive symptoms can be blunted or abated with antidepressant medications”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Hannestad et al., 2011
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- Authors
- Hannestad, J., DellaGioia, N., Ortiz, N., Pittman, B., & Bhagwagar, Z.
- Affiliations
- Yale University (US)
- Corresponding author
- Hannestad, Jonas
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 25
- Issue
- 2
- Pages
- 256-259
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC3025065
- OpenAlex
- W1972187375
- Cited by
- 95
- References
- 25
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 4 · 2023: 4 · 2022: 7 · 2021: 5 · 2020: 5 · 2019: 8 · 2018: 10 · 2017: 7 · 2016: 8 · 2015: 9 · 2014: 3 · 2013: 8 · 2012: 10
- FWCI
- 2.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Center for Research Resources (UL1RR024139)
- 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
- citalopram, endotoxin, fatigue, lassitude, depression, inflammatory cytokines, TNF-α, interleukin-6, innate immune activation, antidepressants, serotonin reuptake inhibitors, social anhedonia, anxiety, mood
- MeSH terms
- Adult, Anxiety, Behavior, Depression, Double-Blind Method, Endotoxins, Fatigue, Female, Humans, Interpersonal Relations, Male, Psychiatric Status Rating Scales, Social Behavior, Citalopram, Cytokines, Selective Serotonin Reuptake Inhibitors
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