Spinal cord injury (SCI) is a life-altering event for which there is no treatment. Depending on injury location and severity, the breadth of the effects can go far past simple mobility. Primary mechanical trauma triggers a variety of secondary cellular events that exacerbate tissue loss as well as facilitate endogenous repair. A large focus of SCI research is on understanding the pathophysiological mechanisms through which these secondary responses contribute to morbidities associated with SCI. Neuroinflammation, a common response to central nervous system (CNS) insult, is central to the secondary injury cascade.
In the context of SCI, the inflammatory response plays a contradictory role in recovery; immune cells release both pro- and anti-inflammatory cytokines at the injury site and clear debris while also causing damage to spared tissue. The major innate and adaptive immune cells that respond to SCI are neutrophils, astrocytes, microglia/macrophages, B cells, and T cells. For each cell type, the timing of the cellular response (in both human and rodent models of SCI), the potential role each cell type plays in the pathophysiology of injury, and the therapeutic implications of targeting each cell type for SCI recovery are discussed.
Local Blockade of Sodium Channels by Tetrodotoxin Ameliorates Tissue Loss and Long-Term Functional Deficits Resulting from Experimental Spinal Cord Injury