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. Author manuscript; available in PMC: 2007 May 14.
Published in final edited form as: J Neuroimmunol. 2006 Dec 26;184(1-2):53–68. doi: 10.1016/j.jneuroim.2006.11.014

Figure 1. Inflammation following stroke.

Figure 1

Brain ischemia is triggers inflammatory responses due to the presence of necrotic cells, generation of reactive oxygen species (ROS) and production of inflammatory cytokines even within neurons. These initiators lead to microglial activation which produce more cytokines causing upregulation of adhesion molecules in the cerebral vasculature. Chemokines lead to inflammatory cell chemotaxis to ischemic brain. Adhesion molecules mediate adhesion of circulating leukocytes to vascular endothelia and infiltration into the brain parenchyma. Once in the brain, activated leukocytes and microglia produce a variety of inflammatory mediators such as matrix metalloproteinases (MMPs), inducible nitric oxide synthase (iNOS) which generates nitric oxide (NO), cytokines and more ROS which lead to brain edema, hemorrhage and ultimately, cell death. MMPs are thought to mediate extracellular matrix disruption, a key event in brain edema and hemorrhage.