Interleukin-1 mediates the behavioral hyperalgesia produced by lithium chloride and endotoxin.
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.
Maier
S F
SF
Department of Psychology, University of Colorado at Boulder 80309-0345.
Wiertelak
E P
EP
Martin
D
D
Watkins
L R
LR
D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D004731:Endotoxins / Q000494:pharmacology; D006358:Hot Temperature; D006930:Hyperalgesia / Q000139:chemically induced*; D007375:Interleukin-1 / Q000494:pharmacology / Q000502:physiology*; D008070:Lipopolysaccharides; D018021:Lithium Chloride / Q000494:pharmacology; D010147:Pain Measurement; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects; D013623:Tail
D004731:Endotoxins; D007375:Interleukin-1; D008070:Lipopolysaccharides; D018021:Lithium Chloride