School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia.
Neurosci Lett. 2011 Jan 10;487(3):363-7. doi: 10.1016/j.neulet.2010.10.057. Epub 2010 Oct 27.
Following the initial impact, spinal cord injury (SCI) triggers a number of inflammatory responses which can exacerbate tissue damage in the cord and impair functional recovery. The involvement of several pro-inflammatory cytokines in the secondary degenerative mechanisms of SCI has been well established, although the role of interleukin-17 (IL-17) remains unclear. In the present study, we used IL-17 knockout (KO) and C57BL/6J wildtype (WT) mice to investigate the effects of IL-17 deficiency on locomotor recovery, lesion size, glial activation and inflammatory cell response following spinal cord contusion injury. Our results show that compared to WT mice, IL-17 KO mice had a significantly smaller lesion size, corresponding with significantly improved locomotor functional recovery following SCI. At 6 weeks after injury, recruitment of B cells, dendritic cells and neutrophils was significantly lower in IL-17 KO than WT mice, however there was no difference in the presence of activated microglia and reactive astrocytes, in the injured spinal cord. These findings suggest that IL-17 is a mediator of secondary degeneration, which contributes to neuroinflammation and hinders functional recovery, though its actions do not affect glial activation following SCI.
在最初的冲击之后，脊髓损伤（SCI）会引发一系列炎症反应，这些反应会加剧脊髓组织损伤，并损害功能恢复。几种促炎细胞因子在 SCI 的继发性退行性机制中的作用已经得到充分证实，尽管白细胞介素-17（IL-17）的作用仍不清楚。在本研究中，我们使用 IL-17 敲除（KO）和 C57BL/6J 野生型（WT）小鼠来研究 IL-17 缺乏对脊髓挫伤损伤后运动功能恢复、损伤大小、神经胶质激活和炎症细胞反应的影响。我们的结果表明，与 WT 小鼠相比，IL-17 KO 小鼠的损伤体积明显较小，SCI 后运动功能恢复明显更好。在损伤后 6 周，IL-17 KO 小鼠的 B 细胞、树突状细胞和中性粒细胞募集明显低于 WT 小鼠，然而，在损伤的脊髓中，活化的小胶质细胞和反应性星形胶质细胞的存在没有差异。这些发现表明，IL-17 是继发性退行性变的介质，它会导致神经炎症，并阻碍功能恢复，尽管它的作用不会影响 SCI 后的神经胶质激活。
