Metal limitation and toxicity at the interface between host and pathogen.

Metal limitation and toxicity at the interface between host and pathogen.
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DOI:
10.1111/1574-6976.12087
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发表时间:
2014-11
影响因子:
11.3
通讯作者:
Skaar EP
Skaar EP
中科院分区:
生物学1区
文献类型:
--
作者:
Becker KW;Skaar EP

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金属是许多对病原体和宿主都至关重要的基本过程所需的辅助因子。它们在负责 DNA 复制和转录、缓解氧化应激和细胞呼吸的酶中协调。然而,过量的过渡金属可能有毒,因为它们能够引起自发的氧化还原循环并破坏正常的代谢过程。脊椎动物已经进化出复杂的机制来限制某些关键金属的可用性,同时用其他金属的抗菌浓度淹没感染部位。为了争夺宿主体内有限的金属,同时防止金属毒性,病原体开发了一系列金属调节、获取和流出系统。本综述将涵盖病原菌识别和应对宿主引起的金属稀缺和毒性的机制。
Metals are required cofactors for numerous fundamental processes that are essential to both pathogen and host. They are coordinated in enzymes responsible for DNA replication and transcription, relief from oxidative stress, and cellular respiration. However, excess transition metals can be toxic due to their ability to cause spontaneous, redox cycling and disrupt normal metabolic processes. Vertebrates have evolved intricate mechanisms to limit the availability of some crucial metals while concurrently flooding sites of infection with antimicrobial concentrations of other metals. To compete for limited metal within the host while simultaneously preventing metal toxicity, pathogens have developed a series of metal regulatory, acquisition, and efflux systems. This review will cover the mechanisms by which pathogenic bacteria recognize and respond to host-induced metal scarcity and toxicity.
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