Journal
BRITISH JOURNAL OF PHARMACOLOGY
Volume 130, Issue 6, Pages 1418-1424Publisher
WILEY
DOI: 10.1038/sj.bjp.0703434
Keywords
inflammatory hyperalgesia; interleukin-1 receptor antagonist; bradykinin; tumour necrosis factor alpha; interleukin-1 beta; interleukin-8; prostaglandin E-2
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1 The effect of IL-1ra on response to intraplantar (i.pl.) injection of LPS, carrageenin, bradykinin, TNF alpha, IL-1 beta, IL-beta, PGE(2) and dopamine was investigated in a model of mechanical hyperalgesia in rats. 2 IL-1ra inhibited hyperalgesic response to LPS, carrageenin, bradykinin, TNF alpha, and IL-1 beta, but not responses to IL-8, PGE(2) and dopamine. 3 A sheep anti-rat IL-1ra serum potentiated response to LPS, carrageenin, bradykinin, TNF alpha and IL-1 beta but not IL-8. 4 Carrageenin and LPS stimulated and production of immunoreactive TNF alpha, IL-1 beta and IL-1ra in the skin of injected paws. 5 The inhibition by IL-1ra of the hyperalgesic response to carrageenin was not affected by antibodies neutralizing IL-4 and IL-10. 6 In mice, IL-1ra inhibited the nociceptive response to i.p. injection of acetic acid. 7 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-1 beta-stimulated eicosanoid production.
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