Repeated social defeat activates dendritic cells and enhances Toll-like receptor dependent cytokine secretion
Open accessAbstract
Stress hormones significantly impact dendritic cell (DC) activation and function, typically in a suppressive fashion. However, a social stressor termed social disruption (SDR) has been shown to induce an increase in inflammatory responses and a state of glucocorticoid resistance in splenic CD11b+ monocytes. These experiments were designed to determine the effects of SDR on DC activation, Toll-like receptor-induced cytokine secretion, and glucocorticoid sensitivity. Compared to cells obtained from control animals, splenic DCs from SDR mice displayed increased levels of MHC I, CD80, and CD44, indicative of an activated phenotype. In addition, DCs from SDR mice produced comparatively higher TNF-alpha, IL-6, and IL-10 in response to in vitro stimulation with LPS and CpG DNA. Increased amounts of TNF-alpha and IL-6 were also evident in SDR DC cultures stimulated with poly(I:C). Furthermore, as shown previously in CD11b+ monocytes, the CD11c+ DCs obtained from SDR mice were glucocorticoid resistant. Taken together, the data suggest that social stress, in the absence of any immune challenge, activates DCs, increases DC cytokine secretion in response to Toll-specific stimuli and renders DCs glucocorticoid resistant.
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Positive ELS/CT history is an independent risk factor for peripheral immune dysregulation and long-term, low-grade inflammatory excess (a pro-inflammatory phenotype) in adulthood.
“There is growing evidence suggesting that positive ELS/CT history is an independent risk factor for peripheral immune dysregulation and long-term, low-grade inflammatory excess (i.e., a pro-inflammatory phenotype) in adulthood (101, 164–172).”
From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [168]
The Discussion (page unavailable) reports that social disruption stress activated dendritic cells and increased their cytokine response in mice, supporting a link between stress and altered immune function. It does not study early-life stress or childhood trauma, establish an independent risk factor, or show persistent low-grade inflammation in adulthood. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThese cells are termed 'primed' because they produce enhanced proinflammatory signaling molecules and bactericidal activity when stimulated with an immune challenge.
“These cells are termed 'primed' because they produce enhanced proinflammatory signaling molecules and bactericidal activity when stimulated with an immune challenge (Bailey et al, 2007;Powell et al, 2009).”
From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Powell et al, 2009
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Self-citation
- Authors
- Powell, N. D., Bailey, M. T., Mays, J. W., Stiner-Jones, L. M., Hanke, M. L., Padgett, D. A., & Sheridan, J. F.
- Affiliations
- The Ohio State University (US)
- Corresponding author
- Powell, Nicole D.
- Sheridan, John F.
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 23
- Issue
- 2
- Pages
- 225-231
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC2711866
- OpenAlex
- W2035552438
- Cited by
- 112
- References
- 48
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 4 · 2023: 2 · 2022: 5 · 2021: 8 · 2020: 5 · 2019: 6 · 2018: 5 · 2017: 5 · 2016: 6 · 2015: 5 · 2014: 7 · 2013: 3 · 2012: 12
- FWCI
- 4.92
- 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
- National Institutes of Health
- National Institute of Mental Health (R01MH046801)
- National Institute of Dental and Craniofacial Research (T32DE014320, T32DE014320-6)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- social defeat, social stress, dendritic cells, Toll-like receptors, cytokine production, glucocorticoid resistance, CD11b+ monocytes, CD11c+ dendritic cells, TNF-α, interleukin-6, IL-10, LPS, CpG DNA, poly(I:C), MHC class I, CD80, CD44, splenic dendritic cells
- MeSH terms
- Analysis of Variance, Animals, Cells, Cultured, Dendritic Cells, Dominance-Subordination, Flow Cytometry, Genes, MHC Class I, Glucocorticoids, Lipopolysaccharides, Male, Mice, Inbred C57BL, Monocytes, Spleen, Stress, Psychological, Tumor Necrosis Factor-alpha, Interleukin-6, Cytokines, Interleukin-10, B7-1 Antigen, Hyaluronan Receptors, CD11b Antigen, CD11c Antigen, Toll-Like Receptors, Mice
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