Staphylococcus aureus is a notorious pathogen causing significant morbidity and mortality worldwide. The ability of S. aureus to survive and replicate within phagocytes such as macrophages represents an important facet of immune evasion and contributes to pathogenesis. The mechanisms by which S. aureus acquires nutrients within host cells to support growth remain poorly characterized. Here, we demonstrate that macrophages infected with S. aureus maintain their dynamic ruffling behavior and consume macromolecules from the extracellular milieu. To support the notion that fluid‐phase uptake by macrophages can provide S. aureus with nutrients, we utilized the pharmacological inhibitors PIK ‐III and Dynasore to impair uptake of extracellular macromolecules. Inhibitor treatment also impaired S. aureus replication within macrophages. Finally, using a mutant of S. aureus that is defective in purine biosynthesis we show that intracellular growth is inhibited unless the macrophage culture medium is supplemented with the metabolite inosine monophosphate. This growth rescue can be impaired by inhibition of fluid‐phase uptake. In summary, through consumption of the extracellular environment macrophages deliver nutrients to phagolysosomal S. aureus to promote bacterial growth.

中文翻译：

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巨噬细胞驱动的营养物输送至吞噬体金黄色葡萄球菌，支持细菌生长。

金黄色葡萄球菌是一种臭名昭著的病原体，在全世界范围内造成显着的发病率和死亡率。金黄色葡萄球菌在巨噬细胞等吞噬细胞内生存和复制的能力代表了免疫逃避的一个重要方面，并有助于发病机制。金黄色葡萄球菌在宿主细胞内获取营养以支持生长的机制仍不清楚。在这里，我们证明感染金黄色葡萄球菌的巨噬细胞保持其动态的波动行为并消耗来自细胞外环境的大分子。为了支持巨噬细胞的液相摄取可以为金黄色葡萄球菌提供营养的观点，我们利用药理学抑制剂 PIK ‐III 和 Dynasore 来削弱细胞外大分子的摄取。抑制剂治疗还损害了巨噬细胞内金黄色葡萄球菌的复制。最后，使用嘌呤生物合成有缺陷的金黄色葡萄球菌突变体，我们表明除非巨噬细胞培养基补充代谢物肌苷单磷酸，否则细胞内生长受到抑制。这种生长拯救可能会因抑制液相吸收而受到损害。总之，通过消耗细胞外环境，巨噬细胞将营养物质输送至吞噬溶酶体金黄色葡萄球菌，以促进细菌生长。