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首页> 外文期刊>Infection and immunity >Staphylococcus aureus Adapts to Oxidative Stress by Producing H2O2-Resistant Small-Colony Variants via the SOS Response
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Staphylococcus aureus Adapts to Oxidative Stress by Producing H2O2-Resistant Small-Colony Variants via the SOS Response

机译：金黄色葡萄球菌通过SOS反应产生抗H2O2的小菌落变体，从而适应氧化应激。

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The development of chronic and recurrent Staphylococcus aureus infections is associated with the emergence of slow-growing mutants known as small-colony variants (SCVs), which are highly tolerant of antibiotics and can survive inside host cells. However, the host and bacterial factors which underpin SCV emergence during infection are poorly understood. Here, we demonstrate that exposure of S. aureus to sublethal concentrations of H2O2 leads to a specific, dose-dependent increase in the population frequency of gentamicin-resistant SCVs. Time course analyses revealed that H2O2 exposure caused bacteriostasis in wild-type cells during which time SCVs appeared spontaneously within the S. aureus population. This occurred via a mutagenic DNA repair pathway that included DNA double-strand break repair proteins RexAB, recombinase A, and polymerase V. In addition to triggering SCV emergence by increasing the mutation rate, H2O2 also selected for the SCV phenotype, leading to increased phenotypic stability and further enhancing the size of the SCV subpopulation by reducing the rate of SCV reversion to the wild type. Subsequent analyses revealed that SCVs were significantly more resistant to the toxic effects of H2O2 than wild-type bacteria. With the exception of heme auxotrophs, gentamicin-resistant SCVs displayed greater catalase activity than wild-type bacteria, which contributed to their resistance to H2O2. Taken together, these data reveal a mechanism by which S. aureus adapts to oxidative stress via the production of a subpopulation of H2O2-resistant SCVs with enhanced catalase production.
机译：慢性和复发性金黄色葡萄球菌感染的发生与被称为小菌落变种（SCV）的缓慢生长的突变体的出现有关，该突变体对抗生素具有高度的耐受性，并且可以在宿主细胞内存活。然而，对于在感染期间SCV出现的基础的宿主和细菌因素知之甚少。在这里，我们证明金黄色葡萄球菌暴露于亚致死浓度的H 2 O 2 会导致对庆大霉素耐药的SCV的种群频率发生特定的，剂量依赖性的增加。时程分析显示，H 2 O 2 暴露引起野生型细胞的抑菌作用，在此期间，SCV在金黄色葡萄球菌种群中自发出现。这是通过诱变的DNA修复途径发生的，该途径包括DNA双链断裂修复蛋白RexAB，重组酶A和聚合酶V。除了通过增加突变率触发SCV出现外，H 2 O 2 也被选作SCV表型，通过降低SCV回复野生型的速率，导致表型稳定性增强，并进一步增加SCV亚群的大小。随后的分析表明，SCVs对H 2 O 2 的毒性作用比野生型细菌明显更强。除血红素营养缺陷型外，耐庆大​​霉素的SCV表现出比野生型细菌更高的过氧化氢酶活性，这使其对H 2 O 2 具有抗性。综上所述，这些数据揭示了金黄色葡萄球菌通过产生具有抗过氧化氢酶作用的H 2 O 2 亚型SCV的亚群而适应氧化应激的机制。

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