Catecholamine-induced suppression of interleukin-1 production

Recent evidence indicates that stress can suppress immune responses and thus increase the severity of viral and neoplastic diseases. Although, the mechanisms for stress-induced modulation of immunologic competence are unclear, neuroendocrine hormones are thought to be involved. A direct suppressive...

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Bibliographic Details
Published inLymphokine research Vol. 5; no. 4; p. 239
Main Authors Koff, W C, Fann, A V, Dunegan, M A, Lachman, L B
Format Journal Article
LanguageEnglish
Published United States 1986
Subjects
Animals
Bucladesine - pharmacology
Epinephrine - pharmacology
Interferon-gamma - pharmacology
Interleukin-1 - antagonists & inhibitors
Interleukin-1 - biosynthesis
Lipopolysaccharides - pharmacology
Macrophage Activation - drug effects
Macrophages - drug effects
Mice
Norepinephrine - pharmacology
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Summary:Recent evidence indicates that stress can suppress immune responses and thus increase the severity of viral and neoplastic diseases. Although, the mechanisms for stress-induced modulation of immunologic competence are unclear, neuroendocrine hormones are thought to be involved. A direct suppressive effect could result from the action of neuroendocrine hormones on lymphokine and monokine release. The central role of interleukin-1 (IL-1) in regulating cellular immune responses to infection and neoplasms stimulated the present study evaluating the effects of neuroendocrine hormones on IL-1 production. Norepinephrine and epinephrine inhibited the capacity of gamma interferon and lipopolysaccharide to stimulate IL-1 production from mouse peritoneal macrophages. Moreover, when intracellular and extracellular levels of IL-1 were quantitated, the studies demonstrated a catecholamine-mediated block in IL-1 synthesis without effect on its release. We also observed that exogenous cyclic AMP (cAMP) administered to mouse macrophages suppressed IL-1 production. This, coupled with the capacity of norepinephrine and epinephrine to enhance intracellular cAMP levels in macrophages, strongly suggested that the catecholamine-induced suppression of IL-1 production may be mediated by elevated intracellular cAMP levels. These findings demonstrate that selected stress-related neuroendocrine hormones can modulate IL-1 production by macrophages and further support the hypothesis that alteration of macrophage function by neuropeptides and neurohormones is a significant feature of stress-induced enhancement of viral and neoplastic disease.
ISSN:0277-6766