Cytokine-mediated inflammatory hyperalgesia limited by interleukin-1 receptor antagonist
Cytokine-mediated inflammatory hyperalgesia limited by interleukin-1 receptor antagonist
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DOI:
10.1038/sj.bjp.0703434
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发表时间:
2000-07-01
影响因子:
7.3
通讯作者:
Ferreira, SH
中科院分区:
文献类型:
--
作者:
Cunha, JM;Cunha, FQ;Ferreira, SH
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.