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首页> 外文期刊>Infection and immunity >Involvement of superoxide and myeloperoxidase in oxygen-dependent killing of Staphylococcus aureus by neutrophils.
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Involvement of superoxide and myeloperoxidase in oxygen-dependent killing of Staphylococcus aureus by neutrophils.

机译：超氧化物和髓过氧化物酶参与中性粒细胞的氧依赖性金黄色葡萄球菌杀伤。

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We have used a quantitative assay that measures independent rate constants for phagocytosis and killing of Staphylococcus aureus to investigate the involvement of superoxide and myeloperoxidase in bacterial killing by human neutrophils. To inhibit superoxide-dependent processes, superoxide dismutase was cross-linked to immunoglobulin G and the conjugate was attached to the surface of S. aureus via protein A in its cell wall. Myeloperoxidase was inhibited with azide, and myeloperoxidase-deficient neutrophils were used. Adding the NADPH oxidase inhibitor diphenyleneiodonium, to prevent superoxide production, decreased the killing rate to 25%, indicating that oxidative killing mechanisms predominate in this system. The rate constant for killing of S. aureus with superoxide dismutase attached was 70% of that for control bacteria linked to inactivated enzyme. Superoxide dismutase had no effect in the presence of diphenyleneiodonium. The rate of killing was decreased to 33% in the presence of azide and to 40% with myeloperoxidase-deficient neutrophils. Superoxide dismutase had no effect in the presence of azide. On the assumption that the oxidative and nonoxidative components of killing can be considered separately, the oxidative rate was decreased by almost half by superoxide dismutase and was about six times lower when myeloperoxidase was inactive. We conclude that myeloperoxidase-dependent processes are strongly favored by human neutrophils as their prime mechanism of oxidative killing of S. aureus and that superoxide makes a direct contribution to killing. Our results also suggest that superoxide acts in conjunction with a myeloperoxidase-dependent pathway.
机译：我们已经使用了一种定量测定法，该测定法测量吞噬作用和金黄色葡萄球菌杀死的独立速率常数，以调查超氧化物和髓过氧化物酶在人类嗜中性粒细胞杀死细菌中的作用。为了抑制超氧化物歧化过程，将超氧化物歧化酶与免疫球蛋白G交联，并将缀合物通过其细胞壁中的蛋白A连接至金黄色葡萄球菌的表面。叠氮抑制了髓过氧化物酶，并使用了髓过氧化物酶缺陷的中性粒细胞。加入NADPH氧化酶抑制剂联苯二碘鎓以防止超氧化物的产生，将杀灭率降低到25％，这表明该系统中氧化杀灭机制占主导地位。附着超氧化物歧化酶杀死金黄色葡萄球菌的速率常数是与灭活酶连接的对照细菌的速率常数的70％。超氧歧化酶在联苯二碘铵的存在下没有作用。在叠氮化物存在下，杀灭率降低到33％，而在缺乏髓过氧化物酶的嗜中性粒细胞中，杀灭率降低到40％。在叠氮化物的存在下，超氧化物歧化酶没有作用。假设可以单独考虑杀灭的氧化和非氧化成分，那么超氧化物歧化酶可使氧化速率降低近一半，而髓过氧化物酶失活时，氧化速率则降低约六倍。我们得出的结论是，人类中性粒细胞强烈依赖于髓过氧化物酶依赖性过程，因为它们是金黄色葡萄球菌氧化杀伤的主要机制，而超氧化物直接导致杀伤。我们的结果还表明，超氧化物与髓过氧化物酶依赖性途径共同起作用。

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