Zinc is an essential cofactor required for life and, as such, mechanisms exist for its homeostatic maintenance in biological systems. Despite the evolutionary distance between vertebrates and microbial life, there are parallel mechanisms to balance the essentiality of zinc with its inherent toxicity. Vertebrates regulate zinc homeostasis through a complex network of metal transporters and buffering systems that respond to changes in nutritional zinc availability or inflammation. Fine-tuning of this network becomes crucial during infections, where host nutritional immunity attempts to limit zinc availability to pathogens. However, accumulating evidence demonstrates that pathogens have evolved mechanisms to subvert host-mediated zinc withholding, and these metal homeostasis systems are important for survival within the host. We discuss here the mechanisms of vertebrate and bacterial zinc homeostasis and mobilization, as well as recent developments in our understanding of microbial zinc acquisition.

中文翻译：

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宿主-病原体界面处的营养锌。

锌是生命所必需的必需辅因子，因此，在生物系统中存在其体内稳态维持的机制。尽管脊椎动物和微生物生命之间存在进化距离，但存在多种平行机制来平衡锌的本质和其固有的毒性。脊椎动物通过复杂的金属转运蛋白和缓冲系统网络调节锌的体内稳态，这些系统对营养锌的可利用性或炎症的变化做出反应。在感染期间，该网络的微调至关重要，宿主的营养免疫力试图限制病原体对锌的利用。但是，越来越多的证据表明，病原体已经进化出了破坏宿主介导的锌扣留的机制，而这些金属稳态系统对于宿主体内的生存很重要。