Abstract
The sickness-inducing agents lithium chloride (LiCl) and lipopolysacharide (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-1 ra) 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-1 ra blocks the hyperalgesia produced by LiCl and LPS.
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