Metal chelation and inhibition of bacterial growth in tissue abscesses
Metal chelation and inhibition of bacterial growth in tissue abscesses
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DOI：
10.1126/science.1152449
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发表时间：
2008-02-15
期刊：
影响因子：
56.9
通讯作者：
Skaar, Eric P.
中科院分区：
文献类型：
--
作者：
Corbin, Brian D.;Seeley, Erin H.;Skaar, Eric P.
细菌感染通常导致组织脓肿的形成，这是入侵细菌与先天免疫系统相互作用的主要部位。我们确定宿主蛋白钙保护蛋白是在金黄色葡萄球菌脓肿中表达的中性粒细胞依赖因子。中性粒细胞来源的钙保护蛋白通过螯合营养Mn2+和Zn2+抑制金黄色葡萄球菌的生长：这种活性导致细菌转录组的重编程。缺乏钙保护蛋白的小鼠脓肿富含金属，葡萄球菌在这些富金属脓肿中增殖增强。这些结果表明钙保护蛋白是感染先天免疫反应的关键因素，并将金属螯合定义为抑制脓肿组织内微生物生长的策略。
Bacterial infection often results in the formation of tissue abscesses, which represent the primary site of interaction between invading bacteria and the innate immune system. We identify the host protein calprotectin as a neutrophil- dependent factor expressed inside Staphylococcus aureus abscesses. Neutrophil- derived calprotectin inhibited S. aureus growth through chelation of nutrient Mn2+ and Zn2+: an activity that results in reprogramming of the bacterial transcriptome. The abscesses of mice lacking calprotectin were enriched in metal, and staphylococcal proliferation was enhanced in these metal- rich abscesses. These results demonstrate that calprotectin is a critical factor in the innate immune response to infection and define metal chelation as a strategy for inhibiting microbial growth inside abscessed tissue.