Inflammatory cell infiltrates have long been observed in the brain following stroke and have largely been thought to mediate recovery and repair. Inflammation is mostly a nonspecific immunologic reaction and is characterized by peripheral leukocyte influx into the cerebral parenchyma and activation of microglia (1,113). Following stroke, necrotic cells and ROS trigger the innate inflammatory response. Ischemic cells, even ischemic neurons, secrete inflammatory cytokines, which can then lead to adhesion-molecule upregulation in the cerebral vascula-ture. Various kinds of brain cells also secrete chemokines, which are involved in recruiting peripheral leukocytes and resident microglia to the ischemic lesion. Inflammatory cells can then generate more inflammatory cytokines and potentially cytotoxic substances, leading to more cell damage, as well as disruption of the BBB and extracellular matrix (Fig. 5) (114). Blocking various aspects of the inflammatory cascade has been shown to ameliorate injury from experimental stroke and suggests an important therapeutic target (113), although this has yet to be demonstrated at the clinical level (115 ).
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