Diet, and specifically dietary metals, can modify the risk of infection. However, the mechanisms by which manganese (Mn), a common dietary supplement, alters infection remain unexplored. We report that dietary Mn levels dictate the outcome of systemic infections caused by Staphylococcus aureus, a leading cause of bacterial endocarditis. Mice fed a high Mn diet display alterations in Mn levels and localization within infected tissues, and S. aureus virulence and infection of the heart are enhanced. Although the canonical mammalian Mn-sequestering protein calprotectin surrounds staphylococcal heart abscesses, calprotectin is not released into the abscess nidus and does not limit Mn in this organ. Consequently, excess Mn is bioavailable to S. aureus in the heart. Bioavailable Mn is utilized by S. aureus to detoxify reactive oxygen species and protect against neutrophil killing, enhancing fitness within the heart. Therefore, a single dietary modification overwhelms vital host antimicrobial strategies, leading to fatal staphylococcal infection.

饮食，特别是饮食中的金属，可以改变感染的风险。然而，常见的膳食补充剂锰 (Mn) 改变感染的机制仍未探索。我们报告说，饮食中的锰水平决定了由金黄色葡萄球菌引起的全身感染的结果，金黄色葡萄球菌是细菌性心内膜炎的主要原因。喂食高锰饮食的小鼠表现出锰水平的改变和受感染组织内的定位，金黄色葡萄球菌的毒力和心脏感染增强。尽管典型的哺乳动物 Mn 螯合蛋白钙卫蛋白围绕着葡萄球菌性心脏脓肿，但钙卫蛋白不会释放到脓肿病灶中，并且不会限制该器官中的 Mn。因此，过量的 Mn 对金黄色葡萄球菌具有生物可利用性在心里。金黄色葡萄球菌利用生物可利用的锰来解毒活性氧并防止中性粒细胞被杀死，从而增强心脏内的健康。因此，单一的饮食改变会压倒重要的宿主抗菌策略，导致致命的葡萄球菌感染。