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Am J Physiol Regul Integr Comp Physiol 273: R1885-R1890, 1997;
0363-6119/97 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 273, Issue 6 1885-R1890, Copyright © 1997 by American Physiological Society

ARTICLES

Epinephrine inhibits endotoxin-induced IL-1 beta production: roles of tumor necrosis factor-alpha and IL-10

T. Van der Poll and S. F. Lowry
Department of Surgery, Cornell University Medical College, New York, New York 10021, USA.

Epinephrine has been found to inhibit the production of the proinflammatory cytokine tumor necrosis factor (TNF)-alpha and to enhance the production of anti-inflammatory cytokine interleukin (IL)-10. To determine the effect of epinephrine on IL-1 beta production, the following experiments were performed: 1) blood obtained from subjects at 4-21 h after the start of a continuous infusion of epinephrine (30 ng.kg-1.min-1) produced less IL-1 beta after ex vivo stimulation with lipopolysaccharide (LPS), compared with blood drawn from subjects infused with saline; 2) in whole blood in vitro, epinephrine caused a dose-dependent decrease in LPS-induced IL-1 beta production, which was likely mediated via adrenergic receptors; and 3) inhibition of TNF and enhancement of IL-10 both contributed to epinephrine-induced inhibition of IL-1 beta production. Epinephrine, either endogenously produced or administered as a component of sepsis treatment, may attenuate excessive activity of proinflammatory cytokines early in the course of systemic infection.


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