Figure 1
Schematic overview of the neuroinflammatory response after ischemic stroke. Microglia become activated after ischemia (grey area) and release pro- and anti-inflammatory mediators. Astrocytes are activated as well and will neglect the maintenance of the neurons, which are most vulnerable to ischemia, and produce neurotoxic and neurotrophic factors. In the ischemic core, neurons die due to necrosis and release necrotic debris into the ischemic tissue, thereby stimulating further activation of glial cells. Astrocytes, together with the attachment of astrocyte endfeet to endothelium and connection with neurons define the neurovascular unit. Neutrophils roll onto the endothelial surface (which is primed by pro-inflammatory cytokines (blue and purple)) until they have slowed down to such a degree that they stick to the endothelium. After binding of selectins to sialyl-Lewisx and CAMs to integrins, the neutrophils undergo conformational changes and flatten. Subsequently, the neutrophils crawl on the endothelium to find an intercellular junction between the endothelial cells for extravasation to the abluminal side and transmigration to the ischemic tissue under the influence of chemokines (red and yellow). Adapted from [26].