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金黄色素与肠杆菌素与髓过氧化物酶和活性氯物种的相互作用。

Interactions of staphyloxanthin and enterobactin with myeloperoxidase and reactive chlorine species.

机构信息

Centre for Free Radical Research, University of Otago Christchurch, P.O. Box 4345, Christchurch, New Zealand.

Department of Pathology & Biomedical Science, University of Otago Christchurch, P.O. Box 4345, Christchurch, New Zealand.

出版信息

Arch Biochem Biophys. 2018 May 15;646:80-89. doi: 10.1016/j.abb.2018.03.039. Epub 2018 Mar 31.

DOI:10.1016/j.abb.2018.03.039
PMID:29614256
Abstract

When neutrophils engulf bacteria, myeloperoxidase converts hydrogen peroxide to hypochlorous acid, which is toxic to all micro-organisms. It has been suggested that some pathogens have virulence factors that target myeloperoxidase to dampen the oxidative reactions of neutrophils. These virulence factors include staphyloxanthin, the golden pigment of Staphylococcus aureus, and enterobactin - a siderophore released by gram-negative bacteria. We investigated the potential of staphyloxanthin and enterobactin to shield bacteria from hypochlorous acid and related chloramines. Clinical strains of S. aureus with high levels of staphyloxanthin and related carotenoids were in general more resistant to low doses of hypochlorous acid than non-pigmented bacteria. But some non-pigmented strains were also resistant to the oxidant. Doses of reactive chlorine species that killed bacteria also bleached their carotenoids. Hypochlorous acid, NHCl, and NHCl bleached purified staphyloxanthin. When S. aureus were phagocytosed by neutrophils there was no discernible loss of staphyloxanthin. These data suggest that staphyloxanthin is capable of protecting bacteria from low doses of reactive chlorine species formed inside phagosomes. Enterobactin was not an inhibitor of myeloperoxidase. We conclude that staphyloxanthin may protect some bacterial strains against oxidative killing by neutrophils, but enterobactin will not inhibit the production of hypochlorous acid.

摘要

当中性粒细胞吞噬细菌时,髓过氧化物酶将过氧化氢转化为次氯酸,次氯酸对所有微生物都有毒性。有人认为,一些病原体具有针对髓过氧化物酶的毒力因子,以抑制中性粒细胞的氧化反应。这些毒力因子包括金黄色葡萄球菌的金黄色素和革兰氏阴性菌释放的铁载体——肠菌素。我们研究了金黄色素和肠菌素保护细菌免受次氯酸和相关氯胺的潜在作用。金黄色葡萄球菌的临床菌株中,高水平的金黄色素和相关类胡萝卜素通常比非色素细菌对低剂量的次氯酸更具抵抗力。但一些非色素菌株也对氧化剂有抵抗力。杀死细菌的活性氯剂量也会使它们的类胡萝卜素褪色。次氯酸、NHCl 和 NHCl 会使纯化的金黄色素褪色。当中性粒细胞吞噬金黄色葡萄球菌时,金黄色素没有明显损失。这些数据表明,金黄色素能够保护细菌免受吞噬体中形成的低剂量活性氯的伤害。肠菌素不是髓过氧化物酶的抑制剂。我们得出结论,金黄色素可能保护某些细菌菌株免受中性粒细胞的氧化杀伤,但肠菌素不会抑制次氯酸的产生。

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