In mechanical injuries like spinal cord and traumatic brain injury or other relatively acute conditions like ischemic reperfusion injury, released damage-associated molecular patterns (DAMPs) induce the innate immune system to activate and produce inflammatory cytokines and reactive oxygen species [58-60]. As previously stated, this response is not purposefully harmful. In fact, it is a necessary step in wound repair [61]. The initial proinflammatory response is to promote killing of any invading organism and remove dead cells to ‘clean’ the damaged area [62]. This response is then shifted to an anti-inflammatory state where debris clearance, extracellular matrix deposition, and angiogenesis are promoted [24]. Thus, when there is proper transition from the M1 to M2 phenotype, the damage can be efficiently repaired. However, when the proinflammatory response does not yield, the constant presence and continued production of inflammatory cytokines and reactive oxygen species can lead to cell death and further tissue damage [63].
