The role of IL-1beta in stress-induced sensitization of proinflammatory cytokine and corticosterone responses - PubMed (original) (raw)

The role of IL-1beta in stress-induced sensitization of proinflammatory cytokine and corticosterone responses

J D Johnson et al. Neuroscience. 2004.

Abstract

Proinflammatory cytokines often sensitize neuronal, hormonal, and behavioral responses to subsequent challenge. Recently, it was observed that exposure to inescapable tailshock enhances peripheral and central proinflammatory cytokine and corticosterone (CORT) responses to subsequent immune challenge up to 4 days later. Thus, we examined the role of central interleukin-1beta (IL-1beta) in stress-induced sensitization of proinflammatory cytokine and CORT responses to a subsequent immune challenge. Rats were administered IL-1 receptor antagonist (IL-1ra) or vehicle into the intra-cisterna magna 1 h prior to tailshock (100, 1.6 mA 5 s shocks) exposure. Twenty-four hours later, rats were challenged i.p. with 10 microg/kg lipopolysaccharide (LPS) and killed 1 h later. IL-1ra had no effect on basal proinflammatory cytokines, but completely blocked the stress-induced enhancement in central and pituitary IL-1beta and plasma IL-6 release following LPS challenge. IL-1ra had no effect on stress-induced enhancement in CORT responses following LPS challenge. Additional rats were administered i.c.v. hrIL-1beta or vehicle and returned to their home cage. Twenty-four hours later, rats were challenged i.p. with either saline or 10 microg/kg LPS and killed 1 h later. Central hrIL-1beta administration significantly elevated central IL-1beta levels and plasma CORT following LPS challenge compared with vehicle-injected controls. These data demonstrate that elevations in central IL-1beta, whether stress-induced or exogenously administered, are sufficient for sensitizing central IL-1beta and CORT responses to subsequent immune challenge. However, during times of stress, exogenous central IL-1ra administration only blocked sensitization of subsequent central IL-1beta responses, not CORT responses, suggesting other factors during the stress response can sensitize CORT responses.

PubMed Disclaimer

Cited by

Inflammation in the pathogenesis of depression: a disorder of neuroimmune origin.
Corrigan M, O'Rourke AM, Moran B, Fletcher JM, Harkin A. Corrigan M, et al. Neuronal Signal. 2023 Jul 13;7(2):NS20220054. doi: 10.1042/NS20220054. eCollection 2023 Jul. Neuronal Signal. 2023. PMID: 37457896 Free PMC article. Review.
Increased alcohol self-administration following repeated Toll-like receptor 3 agonist treatment in male and female rats.
Lovelock DF, Randall PA, Van Voorhies K, Vetreno RP, Crews FT, Besheer J. Lovelock DF, et al. Pharmacol Biochem Behav. 2022 May;216:173379. doi: 10.1016/j.pbb.2022.173379. Epub 2022 Apr 5. Pharmacol Biochem Behav. 2022. PMID: 35395252 Free PMC article.
Ablation of lysozyme M-positive cells prevents aircraft noise-induced vascular damage without improving cerebral side effects.
Frenis K, Helmstädter J, Ruan Y, Schramm E, Kalinovic S, Kröller-Schön S, Bayo Jimenez MT, Hahad O, Oelze M, Jiang S, Wenzel P, Sommer CJ, Frauenknecht KBM, Waisman A, Gericke A, Daiber A, Münzel T, Steven S. Frenis K, et al. Basic Res Cardiol. 2021 Apr 30;116(1):31. doi: 10.1007/s00395-021-00869-5. Basic Res Cardiol. 2021. PMID: 33929610 Free PMC article.
Acute stress induces chronic neuroinflammatory, microglial and behavioral priming: A role for potentiated NLRP3 inflammasome activation.
Frank MG, Fonken LK, Watkins LR, Maier SF. Frank MG, et al. Brain Behav Immun. 2020 Oct;89:32-42. doi: 10.1016/j.bbi.2020.05.063. Epub 2020 May 30. Brain Behav Immun. 2020. PMID: 32485293 Free PMC article.

The role of IL-1beta in stress-induced sensitization of proinflammatory cytokine and corticosterone responses - PubMed (original) (raw)