Catecholamine-induced suppression of interleukin-1 production.

摘要: Recent evidence indicates that stress can suppress immune responses and thus increase the severity of viral neoplastic diseases. Although, mechanisms for stress-induced modulation immunologic competence are unclear, neuroendocrine hormones thought to be involved. A direct suppressive effect could result from action on lymphokine monokine release. The central role interleukin-1 (IL-1) in regulating cellular infection neoplasms stimulated present study evaluating effects IL-1 production. Norepinephrine epinephrine inhibited capacity gamma interferon lipopolysaccharide stimulate production mouse peritoneal macrophages. Moreover, when intracellular extracellular levels were quantitated, studies demonstrated a catecholamine-mediated block synthesis without its We also observed exogenous cyclic AMP (cAMP) administered macrophages suppressed This, coupled with norepinephrine enhance cAMP macrophages, strongly suggested catecholamine-induced suppression may mediated by elevated levels. These findings demonstrate selected stress-related modulate further support hypothesis alteration macrophage function neuropeptides neurohormones is significant feature enhancement disease.