Postischemic inflammatory response. Excitotoxicity and oxidative stress caused by the initial ischemic event activate microglia and astrocytes which react by secreting cytokines, chemokines and matrix metalloproteases (MMP). These inflammatory mediators lead to an upregulation of cell adhesion molecules on endothelial cells, allowing blood-derived inflammatory cells, mainly neutrophils, to infiltrate the ischemic brain area. Neutrophils themselves also secrete cytokines which cause a further activation of glial cells. These processes all result in neuronal cell death and enhance the damage to the ischemic brain.