| First Author | Genovese T | Year | 2009 |
| Journal | J Neurochem | Volume | 108 |
| Issue | 6 | Pages | 1360-72 |
| PubMed ID | 19183262 | Mgi Jnum | J:146854 |
| Mgi Id | MGI:3838682 | Doi | 10.1111/j.1471-4159.2009.05899.x |
| Citation | Genovese T, et al. (2009) Absence of endogenous interleukin-10 enhances secondary inflammatory process after spinal cord compression injury in mice. J Neurochem 108(6):1360-72 |
| abstractText | Interleukin-10 (IL-10) exerts a wide spectrum of regulatory activities in the immune and inflammatory response. The aim of this study was to investigate the role of endogenous IL-10 on the modulation of the secondary events in mice subjected to spinal cord injury induced by the application of vascular clips (force of 24 g) to the dura via a four-level T5-T8 laminectomy. IL-10 wild-type mice developed severe spinal cord damage characterized by oedema, tissue damage and apoptosis (measured by Annexin-V, terminal deoxynucleotidyltransferase-mediated UTP end labeling staining, Bax, Bcl-2, and Fas-L expression). Immunohistochemistry demonstrated a marked increase of localization of TNF-alpha, IL-1beta and S100beta, while western blot analysis shown an increased immunoreactivity of inducible nitric oxide synthase in the spinal cord tissues. The absence of IL-10 in IL-10 KO mice resulted in a significant augmentation of all the above described parameters. We have also demonstrated that the genetic absence of IL-10 worsened the recovery of limb function when compared with IL-10 wild-type mice group (evaluated by motor recovery score). Taken together, our results clearly demonstrate that the presence of IL-10 reduces the development of inflammation and tissue injury events associated with spinal cord trauma. |
