Watson F, Lowe G M, Robinson J J, Galvani D W, Edwards S W
Department of Biochemistry, University of Liverpool.
Biosci Rep. 1994 Apr;14(2):91-102. doi: 10.1007/BF01210304.
Stimulation of the respiratory burst of human neutrophils by fMet-Leu-Phe (in the absence of cytochalasin B) is largely unaffected when the activities of protein kinase C and phospholipase D are inhibited. This has been confirmed using three separate assays to measure the respiratory burst. However, whilst these enzymes are not required for the initiation or maximal rate of oxidant generation, they are required to sustain oxidase activity. In contrast, in the presence of cytochalasin B, fMet-Leu-Phe stimulated oxidase activity is much more dependent on phospholipase D activity. It is proposed that (in the absence of cytochalasin B) activation of the NADPH oxidase utilises cytochrome b molecules that are already present on the plasma membrane and activation occurs independently of phospholipase D and protein kinase C. Once these complexes are inactivated, then new cytochrome b molecules must be recruited from sub-cellular stores. This translocation and/or activation of these molecules is phospholipase D dependent. Some support for this model comes from the finding that the translocation of CD11b (which co-localises with cytochrome b) onto the cell surface is phospholipase D dependent.
在抑制蛋白激酶C和磷脂酶D的活性时，甲酰甲硫氨酰-亮氨酰-苯丙氨酸（fMet-Leu-Phe，在无细胞松弛素B的情况下）对人中性粒细胞呼吸爆发的刺激作用基本不受影响。这一点已通过三种独立的测定方法来测量呼吸爆发得到了证实。然而，虽然这些酶对于氧化剂生成的起始或最大速率并非必需，但它们对于维持氧化酶活性却是必需的。相比之下，在存在细胞松弛素B的情况下，fMet-Leu-Phe刺激的氧化酶活性对磷脂酶D活性的依赖性要强得多。有人提出，（在无细胞松弛素B的情况下）NADPH氧化酶的激活利用的是已经存在于质膜上的细胞色素b分子，且激活过程独立于磷脂酶D和蛋白激酶C发生。一旦这些复合物失活，那么就必须从亚细胞储存库中招募新的细胞色素b分子。这些分子的这种转位和/或激活是依赖磷脂酶D的。这一模型得到了一些支持，即CD11b（与细胞色素b共定位）向细胞表面的转位是依赖磷脂酶D的。
