The role of inflammatory cytokines in the recovery of spinal cord injury: Recent data on NF-κΒ

Spinal cord injury is damage to the spinal cord, resulting from physical trauma as well as other pathological conditions, causing temporary or permanent changes in its function.  SCI demonstrates increased mortality and morbidity placing a great financial burden to health systems worldwide. The physiology of post-injury spinal cord recovery is complicated and includes primary and secondary damage mechanisms. Inflammation and inflammatory cytokines hold a central role in this procedure. This is a review of the existing literature on the role of inflammatory cytokines in the recovery process following spinal cord injury, with emphasis on the role of the transcriptive factor NF-κΒ. NF-κΒ is the ultimate signaling molecule in pathophysiological mechanisms regulated by inflammatory cytokines, such as TNF-α and IL-1β. Its activation includes a complicated network of pathways that interact with one another through several checkpoints. NF-κΒ modification influences gene expression in the post-injury spinal cord and regulates intracellular procedures that mediate the recovery of the neuronal tissue. These procedures include inflammation, cellular death, oxidative stress and myelination of neuraxons. Therapies that affect NF-κΒ-mediated pathways influence the functionality and the prognosis of patients who have sustained a spinal cord injury.