Anti-inflammatory interleukin-10 therapy in CCI neuropathy decreases thermal hyperalgesia, macrophage recruitment, and endoneurial TNF-α expression
Anti-inflammatory interleukin-10 therapy in CCI neuropathy decreases thermal hyperalgesia, macrophage recruitment, and endoneurial TNF-α expression
复制标题
DOI：
10.1016/s0304-3959(97)00148-6
复制
发表时间：
1998-01-01
期刊：
影响因子：
7.4
通讯作者：
Myers, RR
中科院分区：
文献类型：
--
作者：
Wagner, R;Janjigian, M;Myers, RR
单神经病的慢性压迫损伤模型是一种直接的、部分的神经损伤，产生热痛觉过敏。由这种损伤引起的炎症被认为是神经病理学和行为后遗症的重要原因。该研究涉及在慢性压迫性损伤（CCI）病变的部位和时间施用单剂量（250 ng）的白细胞介素-10（IL-10）（一种内源性抗炎肽），以确定IL-10施用是否可以减弱神经对CCI的炎症反应和导致的热痛觉过敏。在IL-10处理的动物中，CCI后（第3、5和9天）热痛觉过敏显著减少。在研究的两个时间点（CCT后2天和5天），这些动物外周神经损伤部位的组织切片中ED-I（募集巨噬细胞的标志物）免疫反应性细胞谱减少。IL-10处理还在第2天降低了促炎细胞因子肿瘤坏死因子α（TNF-α）的免疫反应性细胞谱，但在第5天没有。病变部位神经病理学的定性光学显微镜评估未表明IL-10和载体处理的切片之间存在实质性差异。作者提出，外周神经损伤部位TNF-α和其他促炎细胞因子的初始产生对神经损伤的长期行为结果有重要影响，IL-10治疗可能通过下调神经对损伤的炎症反应来实现这一点。(C)1998年国际疼痛研究协会。出版社：Elsevier Science B. V.
The chronic constriction injury model of mononeuropathy is a direct, partial nerve injury yielding thermal hyperalgesia. The inflammation that results from this injury is believed to contribute importantly to both the neuropathological and behavioral sequelae. This study involved administering a single dose (250 ng) of interleukin-10 (IL-IO), an endogenous anti-inflammatory peptide, at the site and time of a chronic constriction injury (CCI) lesion to determine if IL-10 administration could attenuate the inflammatory response of the nerve to CCI and resulting thermal hyperalgesia. In IL-10-treated animals, thermal hyperalgesia was significantly reduced following CCI (days 3, 5 and 9). Histological sections from the peripheral nerve injury site of those animals had decreased cell profiles immunoreactive for ED-I, a marker of recruited macrophages, at both times studied (2 and 5 days post-CCT). IL-10 treatment also decreased cell profiles immunoreactive for the pro-inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) at day 2, but not day 5. Qualitative light microscopic assessment of neuropathology at the lesion site did not suggest substantial differences between IL-IO and vehicle-treated sections. The authors propose that initial production of TNF-alpha and perhaps other proinflammatory cytokines at the peripheral nerve lesion site importantly influences the long-term behavioral outcome of nerve injury, and that IL-10 therapy may accomplish this by downregulating the inflammatory response of the nerve to injury. (C) 1998 International Association for the Study of Pain. Published by Elsevier Science B.V.