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
Ferreira, SH
中科院分区:
医学2区
文献类型:
--
作者:
Cunha, JM;Cunha, FQ;Ferreira, SH

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1 在大鼠机械性痛觉过敏模型中研究了 IL-1ra 对足底 (i.pl.) 注射 LPS、角叉菜胶、缓激肽、TNF α、IL-1 β、IL-β、PGE(2) 和多巴胺的影响。2 IL-1ra 抑制对 LPS、角叉菜胶、缓激肽、TNF α 和 IL-1 β 的痛觉过敏反应,但不抑制对IL-8、PGE(2) 和多巴胺。3 绵羊抗大鼠 IL-1ra 血清增强对 LPS、角叉菜胶、缓激肽、TNF α 和 IL-1 β 的反应,但不增强对 IL-8.4 角叉菜胶和 LPS 的刺激,并在注射的爪子皮肤中产生免疫反应性 TNF α、IL-1 β 和 IL-1ra。5 IL-1ra 对角叉胶的痛觉过敏反应的抑制不受中和 IL-4 和 IL-10.6 抗体的影响。在小鼠中,IL-1ra 抑制腹腔注射的伤害性反应。注射乙酸。7 这些数据表明,炎症部位释放的 IL-1ra 可以限制炎症性痛觉过敏。这种作用与(IL-1ra 诱导的)IL-4 和 IL-10 无关,并且似乎是 IL-1ra 拮抗 IL-1 β 刺激的类二十烷酸产生的结果。
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.