Abstract
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 non-inflammatory stress play important roles as signal molecules. For example, central administration of interleukin-1β (IL-1β) and interferon-α (IFN-α) 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-1β and IFN-α increases splenic sympathetic nerve activity, and an electrical stimulation of the nerve results in a suppression of splenic NK cell activity through a β-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-1β antibody attenuates the IMB-induced NK suppression, and (4) that hypothalamic IL-1β and IFN-α mRNA is increased after 1 hr IMB. These findings, taken together, suggest that IL-1β and IFN-α produced in the brain may be key substances mediating the IMB stress-induced immunosuppression.