1. Cytokine-mediated inflammatory hyperalgesia limited by interleukin-1 receptor antagonist
- Author
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Joice Maria da Cunha, Fernando Q. Cunha, S Poole, and S. H. Ferreira
- Subjects
Pharmacology ,medicine.medical_specialty ,Lipopolysaccharide ,business.industry ,Bradykinin ,Interleukin ,Inflammation ,chemistry.chemical_compound ,Interleukin 10 ,Interleukin 1 receptor antagonist ,Endocrinology ,chemistry ,Internal medicine ,Hyperalgesia ,medicine ,medicine.symptom ,business ,Interleukin 4 - Abstract
The effect of IL-1ra on response to intraplantar (i.pl.) injection of LPS, carrageenin, bradykinin, TNFα, IL-1β, IL-8, PGE2 and dopamine was investigated in a model of mechanical hyperalgesia in rats. IL-1ra inhibited hyperalgesic response to LPS, carrageenin, bradykinin, TNFα, and IL-1β, but not responses to IL-8, PGE2 and dopamine. A sheep anti-rat IL-1ra serum potentiated response to LPS, carrageenin, bradykinin, TNFα and IL-1β but not IL-8. Carrageenin and LPS stimulated and production of immunoreactive TNFα, IL-1β and IL-1ra in the skin of injected paws. The inhibition by IL-1ra of the hyperalgesic response to carrageenin was not affected by antibodies neutralizing IL-4 and IL-10. In mice, IL-1ra inhibited the nociceptive response to i.p. injection of acetic acid. These data suggest that IL-1ra, released at sites of inflammation, limits inflammatory hyperalgesia. This effect is independent of (IL-1ra-induced) IL-4 and IL-10 and appears to be the result of antagonism by IL-1ra of IL-1β-stimulated eicosanoid production. British Journal of Pharmacology (2000) 130, 1418–1424; doi:10.1038/sj.bjp.0703434
- Published
- 2000
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