Ischemia and neuroimmunology--ischemia/reperfusion injury

Immunological events are implicated in the brain damages after ischemia. Neutrophils have been implicated in the pathogenesis of ischemia-reperfusion injury. We showed beneficial effect of antineutrophol monoclonal antibody RP3, which depletes circulationing neutrophils, on brain edema formation and infarct size. In addition, marked increase in IL-8 concentration was detected in brain and serum during early reperfusion. Time course of IL-8 production precedes brain edema formation and neutrophil infiltration. It is reported that IL-1 induces IL-8 production and anti-IL-1 antibody significantly reduced ischemic brain damages. Neutralizing antibodies against cell adhesion molecules (ICAM-1 and LFA-1) regulate neutrophil: endothel adhesion and monoclonal antibodies against these adhesion molecules reduced the size of infarction. These results indicate that neutrophil infiltration into the ischemic brain is implicated in postischemic brain injury.