IL-1 type I receptor mediates acute phase response to turpentine, but not lipopolysaccharide, in mice.
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.
Leon
L R
LR
Institute for Basic and Applied Medical Research, Lovelace Institutes, Albuquerque, New Mexico 87108, USA.
Conn
C A
CA
Glaccum
M
M
Kluger
M J
MJ
D000210:Acute-Phase Reaction / Q000139:chemically induced*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D006824:Hybridization, Genetic; D007274:Injections, Intraperitoneal; D007279:Injections, Subcutaneous; D007375:Interleukin-1 / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D018345:Mice, Knockout / Q000235:genetics; D017472:Receptors, Interleukin-1 / Q000235:genetics / Q000502:physiology*; D014425:Turpentine / Q000009:adverse effects
D007375:Interleukin-1; D008070:Lipopolysaccharides; D017472:Receptors, Interleukin-1; D014425:Turpentine