Onodera H, Yamasaki Y, Matsuo Y
Department of Neurology, Tohoku University School of Medicine.
Nihon Rinsho. 1994 Nov;52(11):2995-9.
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.
免疫反应与缺血后的脑损伤有关。中性粒细胞与缺血再灌注损伤的发病机制有关。我们发现抗中性粒细胞单克隆抗体RP3(可消耗循环中的中性粒细胞)对脑水肿形成和梗死灶大小具有有益作用。此外,在早期再灌注期间,脑和血清中白细胞介素-8(IL-8)浓度显著升高。IL-8产生的时间进程先于脑水肿形成和中性粒细胞浸润。据报道,白细胞介素-1可诱导IL-8产生,抗白细胞介素-1抗体可显著减轻缺血性脑损伤。针对细胞黏附分子(细胞间黏附分子-1和淋巴细胞功能相关抗原-1)的中和抗体可调节中性粒细胞与内皮细胞的黏附,针对这些黏附分子的单克隆抗体可减小梗死灶大小。这些结果表明,中性粒细胞浸润到缺血脑与缺血后脑损伤有关。