Chemokines tissue-infiltrating cell expression

Inflammatory cells infiltrating postischemic tissue are considered to contribute to disability after cerebral ischemia [5,8,17]. Identification of factors involved in the selective recruitment and accumulation of inflammatory cells into ischemic brain tissue and the mechanisms behind the entry of leukocytes through the blood-brain barrier into sites of ischemia are not completely understood [5,8]. Locally produced proinflammatory cytokines such as TNF-a, IL-1 P, and IL-6 initiate the inflammatory process. TNF-a and IL-1 P mRNA elevate in the brain after experimental middle cerebral artery occlusion [5,51,81]. While, IL-1 p and TNF-a play a major role in promoting adhesion between endothelial cells and leukocytes, they are poor attractants for polymorphonuclear leukocytes and monocytes [7]. Astrocytes and endothelial cells can respond in vitro to such proinflammatory cytokines with enhanced expression of chemokines, which results in the influx of leukocytes to areas of inflammation [5,8,103]. 

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