The central administration of immune cytokines such as interleukin-1 (IL-1) and interferon-α (IFN-α) results in the suppression of peripheral cellular immunity, which depends, at least partly, on the sympathetic nervous activity. An intrathird cerebroventricular (I3V) infusion of recombinant human IL-1β (rhIL-1β) (1-5 ng/rat) elicited a dosedependent increase in the electrical activity of the splenic sympathetic nerve in urethane and α-chloralose anesthetized rats. The effect of rhIL-1β (1 ng/rat) was completely blocked by pretreatment with an IL-1 receptor antagonist (1 μg/rat, I3V 10 min before rhIL-1β), sodium salicylate (1 μg/rat), or α-melanocyte stimulating hormone (α-MSH) (400 ng/rat). Furthermore, an antagonist of corticotropin-releasing factor (CRF), α-helical CRF9.41 (2 μg/rat), completely abolished the rhIL-1β-induced increase in the splenic nerve activity, although an I3V infusion of CRF (1 μg/rat) excited it. These results suggest that IL-1β in the brain activates splenic sympathetic activity by its receptor-mediated and prostaglandin-dependent action that is sensitive to α-MSH, depending on CRF system. Our findings, together with the previous results, suggest that the splenic sympathetic nerve represents one of the communication channels from the brain to the immune system.
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