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首页> 外文期刊>Infection and immunity >Phospholipase A2 Functions in Pseudomonas aeruginosa- Induced Apoptosis
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Phospholipase A2 Functions in Pseudomonas aeruginosa- Induced Apoptosis

机译：铜绿假单胞菌诱导的细胞凋亡中的磷脂酶A2功能

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Pseudomonas aeruginosa, a gram-negative, facultative pathogen, causes severe and often even lethal infections in immunocompromised patients, as well as cystic fibrosis patients. We show here that a variety of P. aeruginosa strains activate phospholipase A2 (PLA2), cultured epithelial cells, and fibroblasts, resulting in increased intracellular and extracellular arachidonic acid release. The use of different PLA2 inhibitors revealed that P. aeruginosa-induced arachidonic acid release is mediated by activation of cytosolic PLA2 (cPLA2), whereas iPLA2 or sPLA2 do not seem to be involved in the response to P. aeruginosa. Likewise, the cPLA2-specific inhibitors MAFP and AACOCF3 prevented apoptosis of cultured epithelial cells upon P. aeruginosa infection, whereas inhibitors specific for iPLA2 or sPLA2 were without effect. The physiological significance of these findings is indicated by an inhibition of apoptosis in tracheal epithelial cells upon in vivo infection with P. aeruginosa. The data indicate that arachidonic acid generation by activation of cPLA2 during P. aeruginosa infection plays an important role in the induction of host cell death.
机译：革兰氏阴性兼性病原菌铜绿假单胞菌在免疫受损的患者以及囊性纤维化患者中引起严重甚至致命的感染。我们在这里显示了各种 P。铜绿假单胞菌菌株激活磷脂酶A 2 （PLA 2 ），培养的上皮细胞和成纤维细胞，导致细胞内和细胞外花生四烯酸释放增加。使用不同的PLA 2 抑制剂可发现 P。铜绿诱导的花生四烯酸释放是通过激活胞质PLA 2 （cPLA2）介导的，而iPLA 2 或sPLA 2 的激活似乎没有参与对 P的回应。铜绿。同样，cPLA 2 特异性抑制剂MAFP和AACOCF3可防止 P时培养的上皮细胞凋亡。铜绿假单胞菌感染，而对iPLA 2 或sPLA 2 特异的抑制剂无效。这些发现的生理学意义通过在体内被 P感染后抑制气管上皮细胞的凋亡来表明。铜绿。数据表明在 P期间通过激活cPLA 2 产生花生四烯酸。铜绿菌感染在诱导宿主细胞死亡中起重要作用。

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