Injuries to the CNS lead to severe and often irreversible deficits in sensorimotor and autonomous function. In spinal cord injury (SCI), mechanical damage results in the death of local neurons and glia at the lesion site within minutes to hours. This is followed by a delayed secondary damage phase characterized by neuronal and glial apoptosis (Liu et al., 1997), an increase in blood–spinal cord barrier (BSB) permeability (Popovich et al., 1996) and a neuroinflammatory response (Fleming et al., 2006) that remains poorly understood. This secondary damage process worsens the outcome and thus should serve as an important target for therapy (Oyinbo, 2011).

The neuroinflammatory response after SCI is mediated by various cell types, including astrocytes, resident microglia, infiltrating immune cells, and endothelial cells, which form the linings of the blood vessels (Hausmann, 2003). The spinal cord has a more pronounced inflammatory response to injury than the brain, with twice as many neutrophils infiltrating within 24 h, a sustained macrophage infiltration, and enhanced lymphocyte infiltration (Schnell et al., 1999). This special property may make the spinal cord particularly vulnerable to secondary lesion processes.