Timecourse and corticosterone sensitivity of the brain, pituitary, and serum interleukin-1 beta protein response to acute stress

Activation of peripheral immune cells leads to increases of interleukin-1 b eta (IL-1 beta) mRNA, immunoreactivity, and protein levels in brain and pit uitary. Furthermore, IL-1 beta in brain plays a role in mediating many of t he behavioral, physiological, and endocrine adjustments induced by immune a ctivation. A similarity between the consequences of immune activation and e xposure to stressors has often been noted, but the potential relationship b etween stress and brain IL-1 beta has received very little attention. A pri or report indicated that exposure to inescapable tailshocks (IS) raised lev els of brain IL-1 beta protein 2 h after IS, but only in adrenalectomized ( and basal corticosterone replaced) subjects. The studies reported here expl ore this issue in more detail. A more careful examination revealed that IL- 1 beta protein levels in hypothalamus were elevated by IS in intact subject s, although adrenalectomy, ADX (with basal corticosterone replacement) exag gerated this effect. IL-1 beta protein increases were already present immed iately after the stress session, both in the hypothalamus and in other brai n regions in adrenalectomized subjects, and no longer present 24 h later. F urthermore, IS elevated levels of IL-1 beta protein in the pituitary, and d id so in both intact and adrenalectomized subjects. IS also produced increa sed blood levels of IL-1 beta, but only in adrenalectomized subjects. Final ly, the administration of corticosterone in an amount that led to blood lev els in adrenalectomized subjects that match those produced by IS, inhibited the IS-induced rise in IL-1 beta in hypothalamus and pituitary, but not in other brain regions or blood. (C) 2000 Elsevier Science B.V. All rights re served.