Spinal cord injury induces lesional expression of the proinflammatory and antiangiogenic cytokine EMAP II.

Inflammatory cellular responses to spinal cord injury are promoted by proinflammatory messengers. We have analyzed expression of endothelial monocyte activating polypeptide II (EMAP II), a proinflammatory, antiangiogenic cytokine in rats after spinal cord injury (SCI) in comparison to normal rat spinal cords. Immunohistochemical analysis demonstrated a highly significant (p < 0.0001) accumulation of EMAP II(+) microglia/macrophages at the lesion site compared to remote areas and uninjured controls. After peaking at day 3, EMAP II(+) microglia/macrophage cell numbers declined gradually until day 28 after SCI-but still remained elevated. Further, EMAP II(+) cells formed clusters in perivascular Virchow-Robin spaces reaching a maximum at day 3. Prolonged accumulation of EMAP II(+), ED1(+) microglia/macrophages suggest a role of EMAP II in the pathophysiology of secondary injury following SCI.