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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Role of p38 in the Priming of Human Neutrophils by Peritoneal Dialysis Effluent
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Role of p38 in the Priming of Human Neutrophils by Peritoneal Dialysis Effluent

机译：p38在腹膜透析流出液引发人类嗜中性粒细胞中的作用

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Peritoneal dialysis effluent (PDE) contains a low-molecular-weight substance that is able to prime human neutrophils for the release of arachidonic acid and superoxide anion. Conventional priming agents, such as tumor necrosis factor alpha (TNF-α), are known to signal via mitogen-activated protein (MAP) kinases; at least one possible substrate for MAP kinases is cytosolic phospholipase A2(cPLA2). Phosphorylation of this enzyme results in arachidonic acid release, and this fatty acid is a potent primer and activator of the human neutrophil NADPH oxidase. Because of the striking similarities between the priming of neutrophils with agents such as TNF-α and PDE, we have investigated the signalling pathways evoked by PDE and explored the possibility that cPLA2 is a target for activated MAP kinases. Our results show that PDE treatment of human neutrophils results in the phosphorylation of the p38 kinase rather than the p42 and p44 kinases. Phosphorylation of p38 is transient with maximal activity being observed 1 min after exposure to PDE. We were unable to demonstrate that activation of p38 resulted in phosphorylation of cPLA2; furthermore, translocation of this enzyme to a membrane-containing fraction was not enhanced in PDE-treated neutrophils. Taken together, these data suggest that, in a manner similar to that of TNF-α, PDE primes human neutrophils by the activation of the p38 kinase. However, unlike the cytokine, the activation of this protein does not result in phosphorylation or activation of cPLA2.
机译：腹膜透析流出物（PDE）包含一种低分子量物质，该物质能够引发人类嗜中性粒细胞释放花生四烯酸和超氧阴离子。已知传统的引发剂，例如肿瘤坏死因子α（TNF-α）通过有丝分裂原激活的蛋白（MAP）激酶发出信号。 MAP激酶的至少一种可能底物是胞质磷脂酶A 2 （cPLA 2 ）。该酶的磷酸化导致花生四烯酸释放，并且该脂肪酸是人嗜中性粒细胞NADPH氧化酶的有效引物和活化剂。由于嗜中性粒细胞与诸如TNF-α和PDE的试剂引发的惊人相似性，我们研究了PDE诱发的信号通路，并探讨了cPLA 2 是激活的MAP激酶的靶标的可能性。我们的结果表明，人中性粒细胞的PDE治疗可导致p38激酶而不是p42和p44激酶的磷酸化。 p38的磷酸化是短暂的，在暴露于PDE 1分钟后观察到最大活性。我们无法证明p38的激活会导致cPLA 2 的磷酸化。此外，在经PDE处理的嗜中性粒细胞中，该酶向含膜部分的转运没有增强。综上所述，这些数据表明，PDE以类似于TNF-α的方式，通过激活p38激酶引发人嗜中性粒细胞。但是，与细胞因子不同，该蛋白的激活不会导致cPLA 2 的磷酸化或激活。

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