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The Journal of Neuroscience, September 1, 2000, 20(17):6473-6477

Induction of Ikappa Balpha mRNA Expression in the Brain by Glucocorticoids: A Negative Feedback Mechanism for Immune-to-Brain Signaling

Ning Quan1, Lingli He1, Wenmin Lai1, Tiansheng Shen1, and Miles Herkenham2

1 Department of Oral Biology, Ohio State University, Columbus, Ohio 43210, and 2 Section on Functional Neuroanatomy, National Institute of Mental Health, Bethesda, Maryland 20892

Peripheral injection of bacterial endotoxin lipopolysaccharide (LPS) induces brain mRNA expression of the proinflammatory cytokines interleukin-1beta (IL-1beta ) and tumor necrosis factor-alpha and the cytokine-responsive immediate-early gene Ikappa Balpha . Peripheral LPS also increases levels of plasma glucocorticoids. Whether the induction of Ikappa Balpha mRNA in the brain after peripheral LPS injection is caused by the feedback action of glucocorticoids has not been determined. In this study, we examined the mRNA expression of Ikappa Balpha and IL-1beta in the rat brain by in situ hybridization histochemistry. Injection of the glucocorticoid agonist dexamethasone induced Ikappa Balpha mRNA expression in the brain in a pattern identical to that of LPS injection. LPS but not dexamethasone also induced IL-1beta mRNA expression. Pretreatment with dexamethasone 30 min before LPS injection enhanced the expression of Ikappa Balpha mRNA in the brain in a dose-dependent manner. Immobilization of rats for 2 hr (which raises glucocorticoid levels) also induced Ikappa Balpha mRNA expression without inducing the expression of IL-1beta . Brain Ikappa Balpha expression induced by peripheral LPS injection was attenuated by pretreatment of rats with the glucocorticoid antagonist RU-486. Finally, increased expression of IL-1beta mRNA in the brain was observed at 4 hr after peripheral LPS injection in adrenalectomized rats compared with sham-operated rats. These results reveal that in the brain glucocorticoids selectively induce Ikappa Balpha mRNA expression, which serves as a negative feedback mechanism for peripheral LPS-induced synthesis of proinflammatory cytokines. Such an inhibitory control mechanism may be important for preventing prolonged expression of proinflammatory cytokines in the brain after peripheral immune challenge.

Key words: glucocorticoid; Ikappa Balpha ; lipopolysaccharide; brain; inflammatory cytokines; interleukin-1

Copyright © 2000 Society for Neuroscience  0270-6474/00/20176473-05$05.00/0


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