Corbin Brian D, Seeley Erin H, Raab Andrea, Feldmann Joerg, Miller Michael R, Torres Victor J, Anderson Kelsi L, Dattilo Brian M, Dunman Paul M, Gerads Russell, Caprioli Richard M, Nacken Wolfgang, Chazin Walter J, Skaar Eric P
Department of Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Science. 2008 Feb 15;319(5865):962-5. doi: 10.1126/science.1152449.
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.
细菌感染常常导致组织脓肿的形成，而组织脓肿是入侵细菌与固有免疫系统相互作用的主要部位。我们确定宿主蛋白钙卫蛋白是一种在金黄色葡萄球菌脓肿内部表达的中性粒细胞依赖性因子。中性粒细胞衍生的钙卫蛋白通过螯合营养物质锰离子（Mn2+）和锌离子（Zn2+）来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。缺乏钙卫蛋白的小鼠的脓肿富含金属，并且在这些富含金属的脓肿中葡萄球菌的增殖增强。这些结果表明，钙卫蛋白是对感染的固有免疫反应中的关键因子，并将金属螯合定义为抑制脓肿组织内微生物生长的一种策略。
