Department of Anesthesiology, University of California, San Diego, La Jolla, CA 92093-0629, USA.
J Peripher Nerv Syst. 2011 Dec;16(4):277-86. doi: 10.1111/j.1529-8027.2011.00362.x.
This 2011 Peripheral Nerve Society plenary lecture reviews the role of axonal transport in neuroimmune communication following peripheral nerve injury, linking focal changes in Schwann cell activation and release of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-α) with subsequent activation and sensitization of ascending sensory neurons and glia which culminate in the neuropathic pain state. New data demonstrate that axonally transported (biotinylated) TNF-α activates and localizes with dorsal horn astrocytes within 96 h after injection into sciatic nerve, and that glial fibrillary acidic protein (GFAP) activation in these glial cells is diminished in TNF receptor 1 knockout mice. The pathophysiology, neuropathology and molecular biology of Wallerian degeneration are also reviewed from a perspective that links it to upregulation of proinflammatory cytokines and the development of neuropathic pain states. Finally, insights into neuroimmune communication provide rationale for new therapy based on interference with the processes of Wallerian degeneration, cytokine signaling and TNF-α protein sequestration.
这篇 2011 年周围神经学会全体演讲综述了轴突运输在周围神经损伤后的神经免疫通讯中的作用，将施万细胞激活和促炎细胞因子肿瘤坏死因子-α (TNF-α) 释放的局部变化与随后上升感觉神经元和胶质细胞的激活和敏化联系起来，最终导致神经病理性疼痛状态。新数据表明，在坐骨神经内注射后 96 小时内，轴突运输的（生物素化）TNF-α 可激活并定位于背角星形胶质细胞，并且这些胶质细胞中的神经胶质纤维酸性蛋白 (GFAP) 激活在 TNF 受体 1 敲除小鼠中减少。从将其与促炎细胞因子的上调和神经病理性疼痛状态的发展联系起来的角度，还回顾了沃勒变性的病理生理学、神经病理学和分子生物学。最后，对神经免疫通讯的深入了解为基于干扰沃勒变性、细胞因子信号和 TNF-α 蛋白隔离过程的新疗法提供了依据。
