Nishioka H, Horiuchi H, Arai H, Kita T
Department of Geriatric Medicine, Kyoto University Graduate School of Medicine, Japan.
FEBS Lett. 1998 Dec 11;441(1):63-6. doi: 10.1016/s0014-5793(98)01526-9.
Lysophosphatidylcholine (LPC) accumulates in inflammatory tissues, where neutrophils are recruited to generate superoxide anions (O2.-). Here, we show that LPC stimulates O2.- generation in human neutrophils and that the activity is inhibited with phosphatidylinositol 3-kinase (PI3 kinase) inhibitors, but not with protein kinase C (PKC) inhibitors. Furthermore, we demonstrate that LPC activates PI3 kinase in neutrophils. Thus, LPC might contribute to host defense by generating O2.- in neutrophils through PI3 kinase activation, but not through PKC activation.
溶血磷脂酰胆碱(LPC)在炎症组织中蓄积,在这些组织中,嗜中性粒细胞被募集以产生超氧阴离子(O2.-)。在此,我们表明LPC刺激人嗜中性粒细胞产生O2.-,并且该活性被磷脂酰肌醇3激酶(PI3激酶)抑制剂抑制,但不被蛋白激酶C(PKC)抑制剂抑制。此外,我们证明LPC在嗜中性粒细胞中激活PI3激酶。因此,LPC可能通过激活PI3激酶而非PKC,在嗜中性粒细胞中产生O2.-,从而有助于宿主防御。