In treating spinal cord injury (SCI), it is important to identify agents that could diminish the inflammatory response that follows primary injury. Human and rodent SCI research shows an increase in neutrophils following injury, yet, little is known about cellular activation post-injury. This study was implemented in dogs with naturallyoccurring SCI resulting from intervertebral disk herniation (IVDH) to characterize the postinjury inflammatory response. Canine SCI parallels human SCI with respect to identifiable contusion with sustained compression; treatment modalities; and histopathic, molecular and magnetic resonance lesion phenotype. However, unlike most human SCI, dogs with IVDH-SCI do not have poly-trauma masking inflammatory responses to the injured cord. Cerebrospinal fluid (CSF), blood, and spinal cord tissue were characterized in dogs with SCI and in healthy controls recruited from Texas A&M University. Metabolite concentrations from CSF were measured using enzyme-linked immunosorbent assays and tandem mass spectrometry. Isolated peripheral blood neutrophil activity and expression of L-selectin were evaluated with flow cytometric analysis. Neutrophils were identified in damaged spinal cords of dogs with severe IVDH. The inflammatory response in dogs with SCI is increased in CSF metabolite profiles. Neutrophil activity in circulation is prolonged, and there is evidence to suggest a canine specific expression of neutrophil L-selectin. This is the first observation of neutrophils in the damaged canine spinal cord. This study demonstrates changes in the peripheral immune cells in an animal model that closely resembles human pathogenesis of neuroinflammation after spinal cord injury.
