Study on the role of lymphocytes on organ failure and disturbed host defense mechanism due to infection and stress

当OK432或缺血刺激诱导肝窦内皮细胞凋亡时，淋巴细胞可引起灌流肝脏的急性损伤，而刀豆蛋白A激活淋巴细胞时，肝细胞产生的过氧化氢诱导肝腺泡中区肝窦内皮细胞凋亡，并诱导肝窦内皮细胞表达HSP72。抗凋亡蛋白Bcl2定位于肝细胞线粒体的内膜和嵴。在严重感染和脓毒症的小鼠模型中，应用Ok432和脂多糖后，自然杀伤细胞和淋巴因子激活的杀伤细胞活性都升高，但淋巴细胞对Fas介导的凋亡非常敏感。

Lympocytes may induce acute injuries of the perfused liver when sinusoidal endothelial cell apoptosis is induced by the administration of OK432 or ischemic challenge, and when lymphocytes are activated by concanavalin A. In the schemic liver, hydrogen peroxide derived from hepatocytes induces sisusoidal endothelial cell apoptosis in the midzone of Liver acinus as well as Hsp 72 expression in sinusoidal endothelial cells. An anti-apoptotic protein Bcl-2 is located in the inner membrane and crista of mitochondria in the hepatocytes. Localization of Bcl-2 is unchanged by the ischemic challenge.In a mouse model of severe infection and sepsis induced consequent administrations of Ok432 and lipopolysaccharide, both natural killer and lymphokine-activated killer activities are elevated, but lymphocytes are very sensitive to Fas-mediated apoptosis.