Absence of endogenous interleukin-10 enhances secondary inflammatory process after spinal cord compression injury in mice

Tiziana Genovese, Emanuela Esposito, Emanuela Mazzon, Rosanna Di Paola, Rocco Caminiti, Placido Bramanti, Alessandro Cappelani, Salvatore Cuzzocrea

Research output: Contribution to journalArticlepeer-review

Abstract

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-α, IL-1β and S100β, 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.

Original languageEnglish
Pages (from-to)1360-1372
Number of pages13
JournalJournal of Neurochemistry
Volume108
Issue number6
DOIs
Publication statusPublished - Mar 2009

Keywords

  • Apoptosis
  • Cytokines
  • Inflammation
  • Interleukin-10
  • Spinal cord injury

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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