Brain Res. 1993 Oct 1;623(2):321-4.

Interleukin-1 mediates the behavioral hyperalgesia produced by lithium chloride and endotoxin.

Maier SF, Wiertelak EP, Martin D, Watkins LR.

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Department of Psychology, University of Colorado at Boulder 80309-0345.

Abstract

The sickness-inducing agents lithium chloride (LiCl) and lipopolysaccharide (LPS) produce a long-lasting facilitation of the nociceptive tailflick reflex. Many of the behavioral and physiological changes produced by illness are mediated by interleukin-1 (IL-1) released from monocytes stimulated by the pathogenic substance. Monocytes also produce an IL-1 receptor antagonist (IL-1ra) which has been sequenced and cloned. The present experiments report that IL-1 can itself produce hyperalgesia as assessed by tailflick to radiant heat, and that recombinant IL-1ra blocks the hyperalgesia produced by LiCl and LPS.

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