Timecourse and corticosterone sensitivity of the brain, pituitary, and serum interleukin-1β protein response to acute stress
Abstract
Activation of peripheral immune cells leads to increases of interleukin-1beta (IL-1beta) mRNA, immunoreactivity, and protein levels in brain and pituitary. Furthermore, IL-1beta in brain plays a role in mediating many of the behavioral, physiological, and endocrine adjustments induced by immune activation. A similarity between the consequences of immune activation and exposure to stressors has often been noted, but the potential relationship between stress and brain IL-1beta has received very little attention. A prior report indicated that exposure to inescapable tailshocks (IS) raised levels of brain IL-1beta protein 2 h after IS, but only in adrenalectomized (and basal corticosterone replaced) subjects. The studies reported here explore this issue in more detail. A more careful examination revealed that IL-1beta protein levels in hypothalamus were elevated by IS in intact subjects, although adrenalectomy, ADX (with basal corticosterone replacement) exaggerated this effect. IL-1beta protein increases were already present immediately after the stress session, both in the hypothalamus and in other brain regions in adrenalectomized subjects, and no longer present 24 h later. Furthermore, IS elevated levels of IL-1beta protein in the pituitary, and did so in both intact and adrenalectomized subjects. IS also produced increased blood levels of IL-1beta, but only in adrenalectomized subjects. Finally, the administration of corticosterone in an amount that led to blood levels in adrenalectomized subjects that match those produced by IS, inhibited the IS-induced rise in IL-1beta in hypothalamus and pituitary, but not in other brain regions or blood.
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GCs are not involved in the initiation of the immediate short-term inflammatory response to stress.
“Importantly, it is quite clear that GCs are not involved in the initiation of this immediate short-term inflammatory response to stress as adrenalectomy potentiates the response (Nguyen et al., 1998) and GC injection before the stressor inhibits it (Nguyen et al., 2000).”
From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Nguyen et al., 2000
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- Authors
- Nguyen, K. T., Deak, T., Will, M. J., Hansen, M. K., Hunsaker, B. N., Fleshner, M., Watkins, L. R., & Maier, S. F.
- Affiliations
- University of Colorado Boulder (US)
- Corresponding author
- Maier, Steven F.
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2000-03
- Volume
- 859
- Issue
- 2
- Pages
- 193-201
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W2104012185
- Cited by
- 143
- References
- 45
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 6 · 2019: 6 · 2018: 4 · 2017: 6 · 2016: 4 · 2015: 8 · 2014: 6 · 2013: 9 · 2012: 6
- FWCI
- 2.30
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01mh045045-12)
- National Institute of Mental Health (MH-00314, MH 50479, MH-45045)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- IL-1β, acute stress, corticosterone, adrenalectomy, hypothalamus, pituitary gland, brain cytokines, stress-immune interaction, corticosteroid feedback
- MeSH terms
- Adrenalectomy, Animals, Brain, Corticosterone, Interleukin-1, Male, Pituitary Gland, Stress, Physiological, Time Factors, Rats, Sprague-Dawley, Rats
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