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Cited by 424Stress Responses and CortisolTryptophan and brain disordersNeuroinflammation and Neurodegeneration Mechanisms

Catecholamines mediate stress-induced increases in peripheral and central inflammatory cytokines

Johnson, J.D., Campisi, J., Sharkey, C.M., Kennedy, S.L., Nickerson, M., Greenwood, B.N., Fleshner, M.·2005·Neuroscience
DOI 10.1016/j.neuroscience.2005.06.090
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Abstract

Proinflammatory cytokines act at receptors in the CNS to alter physiological and behavioral responses. Exposure to stressors increases both peripheral and central proinflammatory cytokines, yet the mechanism(s) of induction remain unknown. Experiments here examined the role of catecholamines in the in vivo induction of proinflammatory cytokines following tailshock stress. Rats were pretreated i.p. with 2.0 mg/kg prazosin (alpha1-adrenoceptor antagonist), 10.0 mg/kg propranolol (beta-adrenoceptor antagonist), or 5.0 mg/kg labetalol (alpha1- and beta-adrenoceptor antagonist) 30 min prior to tailshock exposure and plasma interleukin-1beta (IL-1beta) and IL-6, along with tissue interleukin-1beta from the hypothalamus, hippocampus, and pituitary were measured immediately following stressor termination. Prazosin attenuated stress-induced plasma IL-1beta and IL-6, but had no effect on tissue IL-1beta levels, while propranolol attenuated plasma IL-6 and blocked tissue IL-1beta elevation, and labetalol, which cannot cross the blood-brain barrier, attenuated plasma IL-1beta and IL-6, blocked pituitary IL-1beta, but had no effect on central tissue IL-1beta levels. Furthermore, administration of 50.0 mg/kg N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride, a neurotoxin that lesions neural projections from the locus coeruleus, prevented stress-induced elevation in hippocampal IL-1beta, a region highly innervated by the locus coeruleus, but had no effect on hypothalamic IL-1beta, a region that receives few locus coeruleus projections. Finally, i.p. injection of 5.0 mg/kg isoproterenol (beta-adrenoceptor agonist) was sufficient to induce circulating IL-1 and IL-6, and tissue IL-1beta. These data suggest catecholamines play an important role in the induction of stress-induced proinflammatory cytokines and that beta-adrenoceptors are critical for tissue IL-1beta induction, while both alpha- and beta-adrenoceptors contribute to the induction of plasma cytokines.

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Crossref · 10.1016/j.neuroscience.2005.06.090

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  • Increased sympathetic nervous system activity has been associated with increased inflammation.

    “increased sympathetic nervous system activity38 have been associated with increased inflammation.”

    From Association of depressive disorders, depression characteristics and antidepressant medication with inflammation (2012) · cites this paper as [38]

  • Adrenoceptor antagonists inhibit stress-induced increases in CNS cytokine production.

    “Supporting this conclusion, adrenoceptor antagonists inhibit stress-induced increases in CNS cytokine production (Johnson et al., 2005).”

    From The Stressed CNS: When Glucocorticoids Aggravate Inflammation (2009) · cites this paper as Johnson et al., 2005

  • Catecholamines mediate increases of central and peripheral inflammatory cytokines and activation of the inflammatory nuclear factor κB signaling pathway in response to stress.

    “Catecholamines mediate increases of central and peripheral inflammatory cytokines and activation of the inflammatory nuclear factor κB signaling pathway in response to stress (36).”

    From Stress triggers flare of inflammatory bowel disease in children and adults (2019) · cites this paper as [36]

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Authors
Johnson, J. D., Campisi, J., Sharkey, C. M., Kennedy, S. L., Nickerson, M., Greenwood, B. N., & Fleshner, M.
Affiliations
University of Colorado Boulder (US)
Corresponding author
Johnson, J.D.
ORCID
Venue
Neuroscience
Publisher
Elsevier BV
Published
2005-01
Volume
135
Issue
4
Pages
1295-1307
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/j.neuroscience.2005.06.090
OpenAlex
W2082347869
Cited by
424
References
86
Citations by year
2026: 7 · 2025: 22 · 2024: 16 · 2023: 21 · 2022: 15 · 2021: 23 · 2020: 27 · 2019: 29 · 2018: 12 · 2017: 28 · 2016: 33 · 2015: 21 · 2014: 17 · 2013: 24 · 2012: 19
FWCI
6.42
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
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
catecholamines, inflammatory cytokines, IL-1β, interleukin-6, beta-adrenergic receptors, alpha-adrenergic receptors, locus coeruleus, prazosin, propranolol, labetalol, isoproterenol, hypothalamus, hippocampus, pituitary gland, blood-brain barrier
MeSH terms
Adrenergic alpha-Antagonists, Adrenergic beta-Antagonists, Animals, Brain Chemistry, Catecholamines, Electroshock, Immunohistochemistry, Labetalol, Male, Prazosin, Propranolol, Rats, Inbred F344, Stress, Psychological, Tyrosine 3-Monooxygenase, Cytokines, Rats

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