The pathophysiological role of acute inflammation after spinal cord injury

Traumatic spinal cord injury (SCI) causes irreparable severe motor and sensory dysfunction. Mechanical trauma rapidly leads to blood-spinal cord barrier disruption, neural cell death, axonal damage, and demyelination, followed by a cascade of secondary injury that expands the additional inflammatory reaction at the lesion site. Although the role of inflammation in this phase is complex, a number of studies have suggested that inflammatory responses spread the damage to the surrounding tissue, induce apoptotic cell death, and impair spontaneous regeneration and functional recovery. However, recent advances in experimental technology, such as the depletion antibodies for a specific fraction of inflammatory cells and the genetically engineered mice deficient only in specific cells, suggest the beneficial aspects of inflammatory cells, such as a neuroprotective effect, the removal of cellular debris, and the attenuation of the inflammatory reaction in general. In this review, I summarize our recent findings about the biological role of inflammatory cells, especially infiltrating neutrophils and activated microglia after SCI. A better understanding of the pathophysiological role of inflammation in the acute phase of SCI will aid in the development of therapeutic strategy to enhance the functional recovery after SCI.