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首页> 外文期刊>Infection and immunity >MntABC and MntH Contribute to Systemic Staphylococcus aureus Infection by Competing with Calprotectin for Nutrient Manganese
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MntABC and MntH Contribute to Systemic Staphylococcus aureus Infection by Competing with Calprotectin for Nutrient Manganese

机译：MntABC和MntH与钙卫蛋白竞争营养性锰有助于系统性金黄色葡萄球菌感染

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During infection, vertebrates limit access to manganese and zinc, starving invading pathogens, such as Staphylococcus aureus, of these essential metals in a process termed “nutritional immunity.” The manganese and zinc binding protein calprotectin is a key component of the nutrient-withholding response, and mice lacking this protein do not sequester manganese from S. aureus liver abscesses. One potential mechanism utilized by S. aureus to minimize host-imposed manganese and zinc starvation is the expression of the metal transporters MntABC and MntH. We performed transcriptional analyses of both mntA and mntH, which revealed increased expression of both systems in response to calprotectin treatment. MntABC and MntH compete with calprotectin for manganese, which enables S. aureus growth and retention of manganese-dependent superoxide dismutase activity. Loss of MntABC and MntH results in reduced staphylococcal burdens in the livers of wild-type but not calprotectin-deficient mice, suggesting that these systems promote manganese acquisition during infection. During the course of these studies, we observed that metal content and the importance of calprotectin varies between murine organs, and infection leads to profound changes in the anatomical distribution of manganese and zinc. In total, these studies provide insight into the mechanisms utilized by bacteria to evade host-imposed nutrient metal starvation and the critical importance of restricting manganese availability during infection.
机译：在感染过程中，脊椎动物限制了锰和锌的访问，使这些必需金属的入侵病原体（如金黄色葡萄球菌）处于饥饿状态，称为“营养免疫”。锰和锌结合蛋白钙卫蛋白是养分保持反应的关键组成部分，缺乏这种蛋白的小鼠不会从金黄色葡萄球菌肝脓肿中螯合锰。金黄色葡萄球菌利用以最小化宿主施加的锰和锌饥饿的一种潜在机制是金属转运蛋白MntABC和MntH的表达。我们对mntA和mntH进行了转录分析，结果表明响应钙卫蛋白处理，两个系统的表达均增加。 MntABC和MntH与钙卫蛋白竞争锰，这使金黄色葡萄球菌生长并保留了锰依赖性超氧化物歧化酶活性。 MntABC和MntH的丧失可减少野生型而非钙卫蛋白缺乏的小鼠肝脏中葡萄球菌的负担，这表明这些系统可促进感染过程中锰的获取。在这些研究过程中，我们观察到鼠类器官之间的金属含量和钙卫蛋白的重要性各不相同，并且感染导致锰和锌的解剖分布发生深刻变化。总的来说，这些研究提供了细菌利用细菌逃避宿主施加的营养金属饥饿的机制的深入了解，以及在感染过程中限制锰供应的至关重要性。

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