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

Posttraumatic inflammatory reaction may contribute to secondary injury afte r traumatic spinal cord injury (SCI). Expression of tumor necrosis factor-a lpha (TNF-alpha), a key inflammatory mediator, has been demonstrated in the injured cord. However, the specific cell types that are responsible for TN -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 localize d in neurons, glial cells (including astrocytes, oligodendrocytes, and micr oglia), and endothelial cells in areas of the spinal cord adjacent to the l esion site. Myelin breakdown was noted in oligodendrocytes that are immunop ositive for TNF-alpha. In sham-operated controls, a low level of TNF-alpha immunoreactivity was detected. In antigen-absorption experiments, no TNF-al pha 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, con tribute to TNF-alpha production in the injured cord.