title: Interleukin-1 mediates the behavioral hyperalgesia produced by lithium chloride and endotoxin.
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.
authors.affiliation: Department of Psychology, University of Colorado at Boulder 80309-0345.
authors.forename: S F
authors.initials: SF
authors.lastname: Maier
authors.forename: E P
authors.initials: EP
authors.lastname: Wiertelak
authors.forename: D
authors.initials: D
authors.lastname: Martin
authors.forename: L R
authors.initials: LR
authors.lastname: Watkins
mesh_terms: 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
chemical_list: D004731:Endotoxins; D007375:Interleukin-1; D008070:Lipopolysaccharides; D018021:Lithium Chloride