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

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.