IL-1 type I receptor mediates acute phase response to turpentine, but not lipopolysaccharide, in mice

Am J Physiol. 1996 Dec;271(6 Pt 2):R1668-75. doi: 10.1152/ajpregu.1996.271.6.R1668.


This study examined the role of the interleukin-1 (IL-1) type I receptor (IL-1RtI) in the acute phase response (APR) to inflammation in mice. Turpentine (100 microliters/mouse) injected subcutaneously induced fever, lethargy, body weight loss, and anorexia in IL-1RtI wild-type mice. Knockout mice lacking the IL-1RtI were resistant to these effects of turpentine, supporting a role for this receptor in the APR to local inflammation. The intraperitoneal injection of a low (50 micrograms/kg) or high (2.5 mg/kg) dose of lipopolysaccharide (LPS) induced similar APRs in IL-1RtI wild-type and knockout mice. IL-1RtI knockout mice were resistant to the APR induced by peripherally injected murine IL-1 beta, suggesting that it is not the interaction of endogenous IL-1 beta with IL-1RtII that induces an APR to LPS in these mice. We speculate that the absence of IL-1RtI in these knockout mice results in the sensitization of other cytokine pathways to mediate the APR to LPS.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acute-Phase Reaction / chemically induced*
  • Animals
  • Dose-Response Relationship, Drug
  • Hybridization, Genetic
  • Injections, Intraperitoneal
  • Injections, Subcutaneous
  • Interleukin-1 / pharmacology
  • Lipopolysaccharides* / administration & dosage
  • Male
  • Mice
  • Mice, Inbred Strains
  • Mice, Knockout / genetics
  • Receptors, Interleukin-1 / genetics
  • Receptors, Interleukin-1 / physiology*
  • Turpentine* / adverse effects


  • Interleukin-1
  • Lipopolysaccharides
  • Receptors, Interleukin-1
  • Turpentine