Nutrient transition metals are required cofactors for many proteins to perform functions necessary for life. As such, the concentration of nutrient metals is carefully maintained to retain critical biological processes while limiting toxicity. During infection, invading bacterial pathogens must acquire essential metals, such as zinc, manganese, iron, and copper, from the host to colonize and cause disease. To combat this, the host exploits the essentiality and toxicity of nutrient metals by producing factors that limit metal availability, thereby starving pathogens or accumulating metals in excess to intoxicate the pathogen in a process termed ‘nutritional immunity’. As a result of inflammation, a heterogeneous environment containing both metal-replete and -deplete niches is created, in which nutrient metal availability may have an underappreciated role in regulating immune cell function during infection. How the host manipulates nutrient metal availability during infection, and the downstream effects that nutrient metals and metal-sequestering proteins have on immune cell function, are discussed in this review.

营养过渡金属是许多蛋白质发挥生命所必需功能的辅助因子。因此，营养金属的浓度得到精心维护，以保留关键的生物过程，同时限制毒性。在感染过程中，入侵的细菌病原体必须从宿主那里获得必需的金属，如锌、锰、铁和铜，才能定殖并引起疾病。为了解决这个问题，宿主通过产生限制金属可用性的因素来利用营养金属的重要性和毒性，从而使病原体饥饿或积累过量金属以在称为“营养免疫”的过程中使病原体中毒。作为炎症的结果，产生了包含金属充足和耗尽的生态位的异质环境，其中营养金属的有效性可能在感染期间调节免疫细胞功能方面的作用被低估了。本综述讨论了宿主在感染期间如何操纵营养金属的可用性，以及营养金属和金属螯合蛋白对免疫细胞功能的下游影响。