AJP - Regulatory, Integrative and Comparative Physiology, Vol 266, Issue 5 1670-R1674, Copyright © 1994 by American Physiological Society

ARTICLES

Interleukin-8 induces fever by a prostaglandin-independent mechanism

A. R. Zampronio, G. E. Souza, C. A. Silva, F. Q. Cunha and S. H. Ferreira
Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Universidade de Sao Paulo, Ribeirao Preto, Brazil.

We have studied the mechanism by which interleukin-8 (IL-8) induces fever in rats. Intracerebroventricular injections of IL-8 (5.5-50 ng) evoked dose-dependent increases in body temperature, which reached a plateau 5 h after injection, i.e., later than intracerebroventricular interleukin-1 beta (IL-1 beta; 2 h). The pyrogenic activity of IL-8 was not due to contamination with lipopolysaccharide (LPS) because preincubation of IL-8 with a specific antibody or boiling the IL-8 for 30 min abolished its activity but not that of LPS; also, IL-8 but not LPS induced fever in LPS-tolerant rats. Indomethacin significantly reduced the pyrogenic effects of intracerebroventricular injections of LPS and IL-1 beta but not responses to IL-8, suggesting that pyrogenic responses to IL-8 were mediated independently of prostaglandins. In contrast, dexamethasone markedly attenuated pyrogenic responses to IL-8 and IL-1 beta. These data suggest that inhibition of IL-8 by glucocorticoids contributes to the antipyretic effects of these drugs in fevers resistant to cyclooxygenase inhibitors.

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