Interleukin-17 deficiency improves locomotor recovery and tissue sparing after spinal cord contusion injury in mice

Publication Type:
Journal Article
Citation:
Neuroscience Letters, 2011, 487 (3), pp. 363 - 367
Issue Date:
2011-01-10
Full metadata record
Files in This Item:
Filename Description Size
Thumbnail2010001188OK.pdf404.92 kB
Adobe PDF
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. © 2010 Elsevier Ireland Ltd.
Please use this identifier to cite or link to this item: