Inflammatory mechanism in ischemic neuronal injury

Abstract

Inflammation has been implicated as a secondary mechanism underlying neuronal injury induced by ischemia. A variety of experimental models, including thromboembolic stroke, focal and global ischemia, have been used to evaluate contributions of inflammation to neuronal damage. The vasculature endothelium promotes inflammation through upregulation of adhesion molecules such as intercellular adhesion molecule (ICAM), E-selectin, and P-selectin that bind to circulating leukocytes and facilitate migration of leukocytes into the central nervous system (CNS). Once being in the CNS, leukocytes produce cytotoxic molecules that promote cell death. The response of macrophages and microglia to injury may either be beneficial by scavenging necrotic debris or be detrimental by facilitating cell death of neurons that would otherwise recover. While many studies have tested these hypotheses, the significance of inflammation in stroke models is inconclusive. This review summarizes data regarding roles of cell adhesion molecules, astrocytes, microglia and leukocytes in stroke.