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

Authors
Journal
Brain Research
0006-8993
Publisher
Elsevier
Publication Date
Volume
623
Issue
2
Identifiers
DOI: 10.1016/0006-8993(93)91446-y
Keywords
  • Interleukin-1
  • Interleukin-1 Receptor Antagonist
  • Licl
  • Endotoxin
  • Hyperalgesia
Disciplines
  • Biology

Abstract

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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