Social disruption-induced glucocorticoid resistance: kinetics and site specificity
Abstract
Social disruption (SDR) of male mice has been shown to induce a state of functional glucocorticoid (GC) resistance in splenocytes. The present study demonstrated that GC resistance developed following repeated, but not acute exposure to SDR. GC resistance was long-lasting and persisted for at least 10 days after stress. In contrast, SDR did not alter cytokine secretion from peritoneal mononuclear cells treated with corticosterone. These findings suggest that SDR-induced GC resistance may be restricted to specific sites such as the spleen.
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The repeated and chronic nature of RSD is a critical factor for immune cells to develop GC resistance, as it requires 6 days of social defeat to develop, and persists for at least 10 days after stress termination.
“It should be noted that the repeated and chronic nature of RSD is a critical factor for immune cells to develop GC resistance, as it requires 6 days of social defeat to develop, and persists for at least 10 days after stress termination (Avitsur et al, 2002).”
From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Avitsur et al, 2002
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Self-citation
- Authors
- Avitsur, R., Stark, J. L., Dhabhar, F. S., Padgett, D. A., & Sheridan, J. F.
- Affiliations
- The Ohio State University (US)
- The Ohio State University Wexner Medical Center (US)
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2002-03
- Volume
- 124
- Issue
- 1-2
- Pages
- 54-61
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W2072332068
- Cited by
- 92
- References
- 13
- Citations by year
- 2024: 1 · 2023: 4 · 2022: 4 · 2021: 4 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 4 · 2015: 4 · 2014: 3 · 2013: 1 · 2012: 4
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- John D. and Catherine T. MacArthur Foundation
- National Institutes of Health (1f31mh011792-01)
- National Institute of Mental Health (F31 MH11792, R01MH046801, MH46801-08)
- National Institute of Dental and Craniofacial Research (DE13749-01, P50DE013749)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- social disruption, glucocorticoid resistance, corticosterone, splenocytes, repeated stress, cytokine production, site specificity, stress-induced immunosuppression, male mice
- MeSH terms
- Animals, Cells, Cultured, Corticosterone, Drug Resistance, Interpersonal Relations, Kinetics, Macrophages, Male, Mice, Inbred C57BL, Spleen, Stress, Psychological, Macrophages, Peritoneal, Mice
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