Chemical sympathectomy attenuates lipopolysaccharide-induced increase of plasma cytokine levels in rats pretreated by ACTH

The sympathetic nervous system participates significantly in the regulation of immune functions. In support of this, data indicate that besides vagal afferent and efferent pathway, sympathetic nerves represent crucial component of inflammatory reflex. In addition, it was shown that efferent arm of this reflex might be activated by ACTH. Therefore, we investigated the effect of chemical sympathectomy on lipopolysaccharide (LPS)-induced increases in plasma IL-1 beta, IL-6, and TNF-alpha levels in rats. Plasma IL-10 and corticosterone levels were also evaluated. We also investigated the effect of sympathectomy in rats pretreated with ACTH (1-24). We found that sympathectomy significantly attenuated LPS-induced increases of plasma IL-1 beta levels. Administration of ACTH (1-24) reduced LPS-induced increases of plasma IL-1 beta and IL-6 and exaggerated the rise of IL-10. In animals treated with ACTH (1-24) sympathectomy attenuated LPS-induced increases of IL-1 beta, IL-6, and IL-10 plasma levels. Plasma levels of TNF-alpha and corticosterone were not affected by any interventions. These data indicate that during acute immune challenge, sympathetic nerves stimulate the immune response. In addition, our data indicate that sympathetic nerves are not significantly involved in the anti-inflammatory effect of ACTH (1-24) and that the anti-inflammatory effect of ACTH (1-24) is independent of plasma corticosterone levels.