Cellular localization of tumor necrosis factor-alpha following acute spinal cord injury in adult rats.

Posttraumatic inflammatory reaction may contribute to secondary injury after traumatic spinal cord injury (SCI). Expression of tumor necrosis factor-alpha (TNF-alpha), a key inflammatory mediator, has been demonstrated in the injured cord. However, the specific cell types that are responsible for TNF-alpha expression after SCI remain to be identified. In the present study, cellular sources of TNF-alpha were examined in rats that received a spinal cord impact injury at the 9th thoracic (T9) level. Here we demonstrate that, within hours after SCI, increased TNF-alpha immunoreactivity was localized in neurons, glial cells (including astrocytes, oligodendrocytes, and microglia), and endothelial cells in areas of the spinal cord adjacent to the lesion site. Myelin breakdown was noted in oligodendrocytes that are immunopositive for TNF-alpha. In sham-operated controls, a low level of TNF-alpha immunoreactivity was detected. In antigen-absorption experiments, no TNF-alpha immunoreactivity was detected, indicating the specificity of TNF-alpha immunocytochemistry in the present study. Results suggest that various cell types, including neurons, glial cells, and vascular endothelial cells, contribute to TNF-alpha production in the injured cord.