Hirayama T, Kato I
FEBS Lett. 1983 Jun 27;157(1):46-50. doi: 10.1016/0014-5793(83)81113-2.
The time course experiments of 32Pi-labelling and breakdown of phospholipids in rabbit leukocytes exposed to leukocidin from Pseudomonas aeruginosa suggested that the initial action of this toxin was to stimulate phosphatidic acid production, presumably by causing a rapid metabolic change of phosphatidylinositol (PI response) correlating with phosphatidylinositol-specific phospholipase C and 1,2-diacylglycerol kinase. It appears that a rapid formation of phosphatidic acid and degradation of polyphosphoinositides in leukocytes treated with the toxin might be related a Ca2+-movement from extra- and intracellular spaces, resulting in the activation of Ca2+-dependent enzymes involved in the leukocidic process.
对暴露于铜绿假单胞菌白细胞毒素的兔白细胞中磷脂进行³²P标记和分解的时间进程实验表明,这种毒素的初始作用是刺激磷脂酸的产生,推测是通过引起磷脂酰肌醇的快速代谢变化(PI反应),这与磷脂酰肌醇特异性磷脂酶C和1,2 - 二酰基甘油激酶相关。毒素处理的白细胞中磷脂酸的快速形成和多磷酸肌醇的降解似乎可能与Ca²⁺从细胞外和细胞内空间的移动有关,从而导致参与白细胞杀伤过程的Ca²⁺依赖性酶的激活。