Human focal cerebral infarctions induce differential lesional interleukin-16 (IL-16) expression confined to infiltrating granulocytes, CD8 + T-lymphocytes and activated microglia/macrophages

Focal cerebral ischemia elicits a strong inflammatory response which readily participates in lipid oxygenation, edema formation, apoptotic cell death and tissue remodeling. Within these conditions, cytokines are key players of cell activation and are crucial for delayed mechanisms of ischemic damage. Mature IL-16 is an immunomodulatory cytokine, exerting CD4 dependent and independent effects and is characterized by chemotactic activity, induction of early gene phosphorylation, stimulation of pro-inflammatory IL-1β, IL-6, TNFα expression in monocytic cells and also modulates apoptosis. We have now analyzed expression of IL-16 in 20 brains of patients following focal cerebral infarctions (FCI, n=20). Compared to normal control brains ( n=3), IL-16 was expressed by infiltrating immune cells such as neutrophils, CD8 + lymphocytes and activated CD68 + microglia/macrophages accumulating in lesion associated reactive zones and in peri-vascular regions. IL-16 + cells accumulated significantly ( P