Superoxide production induced in rabbit polymorphonuclear leukocytes by synthetic chemotactic peptides and A23187.
Superoxide production induced in rabbit polymorphonuclear leukocytes by synthetic chemotactic peptides and A23187.
复制标题
合成趋化肽和 A23187 诱导兔多形核白细胞产生超氧化物。
DOI：
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发表时间：
1979
影响因子：
6
通讯作者：
J. Oliver
中科院分区：
文献类型：
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作者：
E. Becker;M. Sigman;J. Oliver
合成甲酰基甲硫基趋化肽诱导呼吸爆发的各种表现：增加0(2)消耗，激活单磷酸己糖分流，增加超氧化物(0（2)(-)）和H(2)0(2)的产生。它们单独起作用，但在细胞松弛素B存在时作用更大。在细胞松弛素B存在时，趋化肽产生的超氧化物表现出结构与活性的相同关系，就像这些试剂刺激趋化运动和趋化性、颗粒酶分泌和中性粒细胞聚集一样。Carbobenzoxy-phenylalanyl-methionine, cbz -ph -met，竞争性地抑制由合成肽引起的运动、颗粒酶分泌和中性粒细胞聚集的诱导刺激。它也是O(2)（-）生成的竞争性抑制剂。结构-活性和竞争性抑制剂的研究得出结论，在多形核白细胞中，趋化肽通过与负责刺激趋化作用、趋化性、颗粒酶分泌和中性粒细胞聚集的相同膜受体相互作用，诱导超氧化物形成，并可能引起呼吸爆发的其他表现。甲酰-蛋氨酸-亮氨酸-苯丙氨酸（f -met -亮氨酸）生成0(2)（-）的效率大大降低，但不会因从外部培养基中去除钙而消失。钙离子载体A23187诱导0(2)（-）的生成，这种生成需要外部钙，并在细胞松弛素b的作用下得到极大增强。根据这些发现，我们假设趋化肽诱导0(2)（-）形成和其他呼吸爆发表现的直接原因是Ca（2+）和/或可能是Na（+）流入中性粒细胞，之前已证明是由肽诱导的。
SYNTHETIC FORMYL METHIONYL CHEMOTACTIC PEPTIDES INDUCE THE VARIOUS MANIFESTATIONS OFTHE RESPIRATORY BURST: increased 0(2) consumption, activation of the hexose mono-phosphate shunt, and increased production of superoxide (0(2) (-)) and H(2)0(2). They do soalone but to a much greater extent when in the presence of cytochalasin B. Superoxidegeneration by the chemotactic peptides in the presence of cytochalasin B shows thesame relationship of structure to activity as does the stimulation of chemokinesis andchemotaxis, granule enzyme secretion, and neutrophil aggregation by these sameagents. Carbobenzoxy-phenylalanyl-methionine, CBZ-Phe-Met, competitively inhibitsthe induced stimulation of locomotion, granule enzyme secretion, and neutrophilaggregation caused by the synthetic peptides. It also is a competitive inhibitor of O(2) (-) generation by the same peptides. The structure-activity and the competitive inhibitor studies lead to the conclusion that in polymorphonuclear leukocytes the chemotactic peptides induce superoxide formation and presumably the other manifestations of the respiratory burst by interacting with the same membrane receptor responsible for the stimulation of chemokinesis, chemotaxis, granule enzyme secretion, and neutrophil aggregation. The effectiveness of formyl-methionyl-leucyl-phenylalanine, F-Met-Leu-Phe, in generating 0(2) (-) is greatly reduced but not abolished by removing calcium from the external medium. The calcium ionophore A23187 induces 0(2) (-) generation that requires external calcium and is greatly enhanced by cytochalasin B. From these findings we hypothesize that the proximate cause of the induction of 0(2) (-) formation and other manifestations of the respiratory burst by the chemotactic peptides is the influx into the neutrophil of Ca(2+) and/or possibly Na(+) previously shown to be induced by the peptides.