Alexander Jessica K, Popovich Phillip G
The Ohio State University College of Medicine, Columbus, OH, USA.
Prog Brain Res. 2009;175:125-37. doi: 10.1016/S0079-6123(09)17508-8.
Traumatic spinal cord injury triggers a complex local inflammatory reaction capable of enhancing repair and exacerbating pathology. The composition and effector potential of the post-injury cellular and molecular immune cascade changes as a function of time and distance from the lesion. Production along this time-space continuum of cytokines, proteases, and growth factors establishes dynamic environments that lead to the death, damage, repair or growth of affected neurons and glia. Microenvironmental cues, therefore, generated by the cells therein, may determine these distinct fates of repair versus pathology. To harness repair, it is necessary to manipulate the assembly and phenotype of cells that comprise the neuroinflammatory response to injury. Here, the potential of the neuroinflammatory response to cause outcomes such as pain, regeneration, and functional recovery is reviewed.
创伤性脊髓损伤引发复杂的局部炎症反应，这种反应既能促进修复，也会加剧病理变化。损伤后细胞和分子免疫级联反应的组成及效应潜能会随时间以及与损伤部位的距离而变化。在这个时空连续体中，细胞因子、蛋白酶和生长因子的产生构建了动态环境，导致受影响的神经元和神经胶质细胞死亡、受损、修复或生长。因此，其中的细胞产生的微环境信号可能决定修复与病理变化这些截然不同的结果。为了促进修复，有必要操控构成对损伤的神经炎症反应的细胞组装和表型。在此，我们综述了神经炎症反应引发疼痛、再生和功能恢复等结果的可能性。
