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The sympathetic nervous system is one of the multiple channels that communicate between brain and immune system. In the brain-immune interactions, cytokines produced in the periphery and brain during inflammatory as well as noninflammatory stress play important roles as signal molecules. For example, central administration of interleukin-1 (IL-1 ) and interferon(IFN) suppresses splenic natural killer (NK) cell activity in rats, which is mediated by, at least in part, the sympathetic innervations to the spleen. The central administration of IL-1 and IFNincreases splenic sympathetic nerve activity, and an electrical stimulation of the nerve results in a suppression of splenic NK cell activity through a -adrenergic receptor-mediated process. Furthermore, it has been shown (1) that immobilization (IMB) stress produces an elevation of extracellular concentration of noradrenaline in the spleen, (2) that the IMB-induced reduction of splenic NK activity is partially blocked by splenic denervation, (3) that pretreatment with central injection of neutralizing anti-IL-1 antibody attenuates the IMB-induced NK suppression, and (4) that hypothalamic IL-1 and IFNmRNA is increased after 1 hr IMB. These findings, taken together, suggest that IL-1 and IFNproduced in the brain may be key substances mediating the IMB stress-induced

Hypothalamo-Sympathetic Modulation of Splenic Natural Killer Cell Activity: An Involvement of Brain Cytokines