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首页> 外文期刊>Journal of Cellular Physiology >Regulation of human eosinophil NADPH oxidase activity: a central role for PKCdelta.
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Regulation of human eosinophil NADPH oxidase activity: a central role for PKCdelta.

机译：人类嗜酸性粒细胞NADPH氧化酶的监管活动:PKCdelta的核心作用。

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Eosinophils play a primary role in the pathophysiology of asthma. In the lung, the activation state of the infiltrating eosinophils determines the extent of tissue damage. Interleukin-5 (IL-5) and leukotriene B4 (LTB4) are important signaling molecules involved in eosinophil recruitment and activation. However, the physiological processes that regulate these activation events are largely unknown. In this study we have examined the mechanisms of human eosinophil NADPH oxidase regulation by IL-5, LTB4, and phorbol ester (PMA). These stimuli activate a Zn2+-sensitive plasma membrane proton channel, and treatment of eosinophils with Zn2+ blocks superoxide production. We have demonstrated that eosinophil intracellular pH is not altered by IL-5 activation of NADPH oxidase. Additionally, PKCdelta inhibitors block PMA, IL-5 and LTB4 mediated superoxide formation. Interestingly, the PKCdelta-selective inhibitor, rottlerin, does not block proton channel activation by PMA indicating that the oxidase and the proton conductance are regulated at distinct phosphorylation sites. IL-5 and LTB4, but not PMA, stimulated superoxide production is also blocked by inhibitors of PI 3-kinase indicating that activation of this enzyme is an upstream event common to both receptor signaling pathways. Our results indicate that the G-protein-coupled LTB4 receptor and the IL-5 cytokine receptor converge on a common signaling pathway involving PI 3-kinase and PKCdelta to regulate NADPH oxidase activity in human eosinophils. Copyright 2001 Wiley-Liss, Inc.
机译：嗜酸性粒细胞中发挥主要作用哮喘的病理生理学。浸润嗜酸性粒细胞的活化状态决定了组织损伤的程度。Interleukin-5 (IL-5)和白三烯B4 (LTB4)是重要的信号分子参与嗜酸性粒细胞招聘和激活。这些生理过程的调节激活事件在很大程度上是未知的。我们已经研究了人类的机制研究嗜酸性粒细胞NADPH氧化酶IL-5监管,LTB4,佛波醇酯(PMA)。激活Zn2 +敏感的质膜质子通道,和治疗嗜酸性粒细胞Zn2 +块过氧化物生产。表明,嗜酸性粒细胞胞内pH值不改变IL-5 NADPH氧化酶的活化。此外,PKCdelta抑制剂阻断PMA, IL-5和LTB4介导超氧化物的形成。有趣的是,PKCdelta-selective抑制剂,rottlerin并不阻止质子通道PMA表明氧化酶和激活质子导电性不同的监管磷酸化的网站。PMA,刺激过氧化物生产也被抑制剂的π3-kinase指示这种酶的激活是一个上游事件共同受体信号通路。我们的结果表明,G-protein-coupledLTB4受体和IL-5细胞因子受体聚集在一个共同的信号通路有关π3-kinase PKCdelta调节NADPH氧化酶活动在人类嗜酸性粒细胞。2001 Wiley-Liss, Inc。

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