Nociceptive and inflammatory effects of subcutaneous TNFalpha.
Nociceptive and inflammatory effects of subcutaneous TNFalpha.
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作者：
H. Junger;L. Sorkin
肿瘤坏死因子α（TNF）是一种强效促炎细胞因子，可在注射后产生疼痛和痛觉过敏。其镇痛作用是由于对伤害性初级传入神经的致敏作用以及其他促炎蛋白和镇痛蛋白的上调。在麻醉大鼠中，我们研究了皮下注射TNF对腓肠神经C伤害感受器的背景活动和机械敏感性的影响，以及其对皮肤血浆外渗的影响。TNF致敏C伤害感受器的剂量依赖性;最佳剂量（5 ng）降低阈值在66.7%的测试纤维。这种致敏作用在30分钟内发生，并可能持续2小时或更长时间。注射TNF对Abeta机械感受性纤维没有影响。此外，TNF诱发了14%的C伤害感受器的持续活动，并引起无毛皮肤血管通透性的显著和剂量相关性增加。我们的数据表明，肿瘤坏死因子释放过程中或组织损伤参与痛觉过敏和炎症的产生。
Tumor necrosis factor alpha (TNF) is a potent pro-inflammatory cytokine that produces pain and hyperalgesia following injection. Its algesic effects are due to sensitizing actions on nociceptive primary afferents and to the upregulation of other pro-inflammatory and algesic proteins. In anesthetized rats, we investigated the effect of subcutaneously injected TNF on background activity and mechanical sensitivity of C nociceptors of the sural nerve, as well as its effects on cutaneous plasma extravasation. TNF sensitized C nociceptors dose-dependently; the optimal dose (5 ng) lowered threshold in 66.7% of the tested fibers. This sensitization occurred within 30 min and could last for 2 or more hours. Injected TNF had no effect on Abeta mechanoreceptive fibers. In addition, TNF evoked ongoing activity in 14% of C nociceptors and caused significant and dose-related increases in vascular permeability in glabrous skin. Our data suggest that TNF released during disease or after tissue injury participates in the generation of hyperalgesia and inflammation.