Inflammatory mechanisms after ischemia and stroke

Inflammation has been implicated as a secondary injury mechanism following ischemia and stroke. A variety of experimental models, including thromboembolic stroke, focal and global ischemia, have been used to evaluate the importance of inflammation. The vasculature endothelium promotes inflammation through the upregulation of adhesion molecules such as ICAM, E-selectin, and P-selectin that bind, to circulating leukocytes and facilitate their migration into the CNS. Once in the CNS, the production of cytotoxic molecules may facilitate cell death. The macrophage and microglial response to injury may either be beneficial by scavenging necrotic debris or detrimental by facilitating cell death in neurons that would otherwise recover. While many studies have tested these hypotheses, the importance of inflammation in these models is inconclusive. This review summarizes data regarding the role of the vasculature, leukocytes, blood-brain barrier, macrophages, and microglia after experimental and clinical stroke.