Social stress increases the susceptibility to endotoxic shock
Abstract
The influence of social disruption stress (SDR) on the susceptibility to endotoxic shock was investigated. SDR was found to increase the mortality of mice when they were challenged with the bacterial endotoxin lipopolysaccharide (LPS). Histological examination of SDR animals after LPS injection revealed widespread disseminated intravascular coagulation in the brain and lung, extensive meningitis in the brain, severe hemorrhage in the lung, necrosis in the liver, and lymphoid hyperplasia in the spleen, indicating inflammatory organ damage. In situ hybridization histochemical analysis showed that the expression of the glucocorticoid receptor mRNA was down-regulated in the brain and spleen of SDR animals while the ratio of expression of AVP/CRH-the two adrenocorticotropic hormone secretagogue, increased. After LPS injection, the expression of pro-inflammatory cytokines, IL-1beta and TNF-alpha, was found significantly higher in the lung, liver, spleen, and brain of the SDR mice as compared with the LPS-injected home cage control animals. Taken together, these results show that SDR stress increases the susceptibility to endotoxic shock and suggest that the development of glucocorticoid resistance and increased production of pro-inflammatory cytokines are the mechanisms for this behavior-induced susceptibility to endotoxic shock.
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Social disruption stress in mice leads to glucocorticoid resistance in splenic monocytes that is associated with increased susceptibility to the lethal effects of inflammatory stimuli, including endotoxic shock and pulmonary virus infection.
“Social disruption stress in mice has been shown to lead to glucocorticoid resistance in splenic monocytes that is associated with increased susceptibility to the lethal effects of inflammatory stimuli, including endotoxic shock and pulmonary virus infection.58,59”
From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [58]
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- Authors
- Quan, N., Avitsur, R., Stark, J. L., He, L., Shah, M., Caligiuri, M., Padgett, D. A., Marucha, P. T., & Sheridan, J. F.
- Affiliations
- The Ohio State University (US)
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2001-04
- Volume
- 115
- Issue
- 1-2
- Pages
- 36-45
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W1988662978
- Cited by
- 177
- References
- 3
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 1 · 2022: 3 · 2021: 5 · 2020: 6 · 2019: 1 · 2018: 8 · 2017: 7 · 2016: 9 · 2015: 6 · 2014: 3 · 2013: 3 · 2012: 10
- FWCI
- 5.66
- 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
- National Institute of Mental Health (R01MH046801, R01-MH46801)
- National Institute of Dental and Craniofacial Research (P50 DE-13749, P50DE013749)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
- Keywords
- social stress, endotoxic shock, lipopolysaccharide, glucocorticoid resistance, glucocorticoid receptor, vasopressin, corticotropin-releasing factor, inflammatory cytokines, IL-1β, TNF-α, disseminated intravascular coagulation, meningitis, lymphoid hyperplasia, neuroimmune interactions
- MeSH terms
- Animals, Cell Division, Cell Separation, Corticosterone, Disease Models, Animal, Disease Susceptibility, Dose-Response Relationship, Drug, Immunocompetence, Interleukin-1, Lipopolysaccharides, Male, Mice, Inbred C57BL, Organ Specificity, Receptors, Glucocorticoid, RNA, Messenger, Shock, Septic, Social Behavior, Spleen, Stress, Physiological, Tumor Necrosis Factor-alpha, Survival Rate, Mice
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