NADPH氧化酶抑制剂二亚苯基碘鎓对人中性粒细胞需氧和厌氧杀菌活性的影响。
The effect of the NADPH oxidase inhibitor diphenyleneiodonium on aerobic and anaerobic microbicidal activities of human neutrophils.
作者信息
Ellis J A, Mayer S J, Jones O T
机构信息
Department of Biochemistry, Medical School, University of Bristol, U.K.
出版信息
Biochem J. 1988 May 1;251(3):887-91. doi: 10.1042/bj2510887.
Abstract
NADPH-dependent superoxide production by intact human neutrophils is inhibited by DPI (diphenyleneiodonium), when stimulated by either FMLP (N-formylmethionyl-leucyl-phenylalanine) or PMA (phorbol 12-myristate 13-acetate). Addition of 10 microM-DPI abolished the reduction of both the FAD and the cytochrome b components of the NADPH oxidase. DPI inhibition of the oxidase was associated with defective aerobic killing of staphylococci by human neutrophils. Anaerobic killing, phagocytosis, chemotaxis and motility were relatively unaffected by 10 microM-DPI. Degranulation of the azurophil and specific granules, induced by the soluble stimuli FMLP or PMA, and by particulate stimuli was decreased by the presence of DPI. The above effects of DPI on human neutrophils are similar to those found in chronic granulomatous disease.
摘要
当完整的人类中性粒细胞受到FMLP（N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸）或PMA（佛波醇12-肉豆蔻酸酯13-乙酸酯）刺激时，其NADPH依赖性超氧化物生成会被DPI（二苯基碘鎓）抑制。添加10微摩尔/升的DPI消除了NADPH氧化酶的FAD和细胞色素b成分的还原。DPI对氧化酶的抑制与人类中性粒细胞对葡萄球菌的需氧杀伤缺陷有关。厌氧杀伤、吞噬作用、趋化性和运动性相对不受10微摩尔/升DPI的影响。由可溶性刺激物FMLP或PMA以及颗粒性刺激物诱导的嗜天青颗粒和特异性颗粒的脱粒，因DPI的存在而减少。DPI对人类中性粒细胞的上述影响与慢性肉芽肿病中的情况相似。
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