The DOI matches its Crossref record; 25 of the 27 references it cites were found in a registry or an index.
Inflammation and social experience: An inflammatory challenge induces feelings of social disconnection in addition to depressed mood
Open accessAbstract
Although research has established links between feelings of social isolation and inflammation, the direction of these effects is unclear. Based on the role that proinflammatory cytokines play in initiating "sickness behavior," which includes symptoms such as social withdrawal, it is possible that inflammatory processes heighten feelings of 'social disconnection.' Here, we examined whether exposure to an inflammatory challenge increased self-reported feelings of social disconnection. In addition, because both inflammatory processes and feelings of social disconnection contribute to depressive symptoms, we also explored whether increases in feelings of social disconnection played a role in the link between inflammation and depressed mood. Participants were randomly assigned to either receive endotoxin, an inflammatory challenge, or placebo. Proinflammatory cytokines (IL-6, TNF-alpha) were collected at baseline and then hourly for 6h. Participants completed self-reports of sickness symptoms ("fatigue"), social disconnection ("I feel disconnected from others"), and depressed mood ("unhappy") hourly. Results revealed that endotoxin led to significant increases (from baseline) in IL-6 and TNF-alpha levels as well as feelings of social disconnection and depressed mood. Moreover, controlling for increases in social disconnection eliminated the relationship between exposure to inflammatory challenge and depressed mood. This study demonstrates that inflammation can have social psychological consequences, which may play a role in cytokine-related depressive symptoms.
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“Specifically, endotoxin administration in healthy controls increases IL-6 and TNF-α levels (Eisenberger et al, 2010) and amygdala response to socially threatening stimuli (Harrison et al, 2009b;Inagaki et al, 2012).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Eisenberger et al, 2010
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Cites
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“…it would be interesting to examine whether inflammatory activity also decreases the sense that one is socially supported, as a perceived lack of social support is a risk factor for both endogenous and cytokineassociated forms of depression (Capuron et al., 2004; Heinrich and Gullone, 2006).”
InfluentialGender differences in depression
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Slavich, G. M., & Irwin, M. R. (2014) · Psychological Bulletin · doi:10.1037/a0035302 · Cited by 2,206
Self-citationRaison, C. L., Rutherford, R. E., Woolwine, B. J., Shuo, C., Schettler, P., Drake, D. F., Haroon, E., & Miller, A. H. (2013) · JAMA Psychiatry · doi:10.1001/2013.jamapsychiatry.4 · Cited by 1,617
Why Sleep Is Important for Health: A Psychoneuroimmunology Perspective
Irwin, M. R. (2015) · Annual Review of Psychology · doi:10.1146/annurev-psych-010213-115205 · Cited by 1,325
“Third, experimental activation of inflammation induces increases of depressive symptoms along with activation of brain sites that regulate positive and negative affect (Eisenberger et al. 2009, 2010a,b).”
BackgroundSelf-citationEisenberger, N. I. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3231 · Cited by 1,016
Self-citationInflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond
Michopoulos, V., Powers, A., Gillespie, C. F., Ressler, K. J., & Jovanovic, T. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.146 · Cited by 786
Metadata
- Authors
- Eisenberger, N. I., Inagaki, T. K., Mashal, N. M., & Irwin, M. R.
- Affiliations
- University of California, Los Angeles (US)
- Northwestern University (US)
- Corresponding author
- Eisenberger, Naomi I.
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 24
- Issue
- 4
- Pages
- 558-563
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC2856755
- OpenAlex
- W2161296293
- Cited by
- 413
- References
- 27
- Citations by year
- 2026: 32 · 2025: 25 · 2024: 24 · 2023: 25 · 2022: 33 · 2021: 38 · 2020: 26 · 2019: 21 · 2018: 28 · 2017: 20 · 2016: 27 · 2015: 24 · 2014: 25 · 2013: 14 · 2012: 26
- FWCI
- 7.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Dana Foundation
- National Institute on Aging (AG 026364, R01AG026364, R01AG034588, P30AG028748)
- National Heart, Lung, and Blood Institute (HL 079955, R01HL079955)
- National Institute of Mental Health (T32MH019925, T32 MH 19925)
- National Cancer Institute (R01CA116778, CA-10014152, CA-116778)
- National Center for Research Resources ((M01 RR00865), M01RR000865)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- inflammation, social disconnection, social isolation, endotoxin, sickness behavior, inflammatory cytokines, interleukin-6, TNF-α, depressive mood, depressive symptoms, fatigue, social withdrawal
- MeSH terms
- Adolescent, Adult, Depression, Double-Blind Method, Endotoxins, Fatigue, Female, Humans, Inflammation, Interpersonal Relations, Male, Social Behavior, Tumor Necrosis Factor-alpha, Interleukin-6, Young Adult
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