Lesional expression of a proinflammatory and antiangiogenic cytokine EMAP II confined to endothelium and microglia/macrophages during secondary damage following experimental traumatic brain injury.

We analyzed expression of Endothelial Monocyte-Activating Polypeptide II (EMAP II), a proinflammatory, antiangiogenic cytokine in rat brains after stab wound injury and observed a highly significant (p<0.0001) lesional accumulation confined to microglia/macrophages. Maximum numbers were seen at day 5 declining until 21 days after injury. Further, EMAP II(+) microglia/macrophages formed clusters in perivascular Virchow-Robin spaces. Prolonged accumulation of EMAP II(+), ED1(+) microglia/macrophages and increased lesional numbers of EMAP II(+) endothelial/smooth muscle cells during the acute postinjury period might indicate that EMAP II enrich the proinflammatory and antiangiogenic repertoire of effector molecules expressed by activated microglia/macrophages during secondary damage.