Iron Acquisition Systems of Gram-negative Bacterial Pathogens Define TonB-Dependent Pathways to Novel Antibiotics.

Iron Acquisition Systems of Gram-negative Bacterial Pathogens Define TonB-Dependent Pathways to Novel Antibiotics.
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DOI:
10.1021/acs.chemrev.0c01005
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发表时间:
2021-05-12
期刊:
影响因子:
62.1
通讯作者:
Chakravorty S
Chakravorty S
中科院分区:
化学1区
文献类型:
--
作者:
Klebba PE;Newton SMC;Six DA;Kumar A;Yang T;Nairn BL;Munger C;Chakravorty S

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铁是原核生物和真核生物中不可或缺的代谢辅因子,在细菌病原体和它们的人类或动物宿主之间产生了对金属的自然竞争。细菌分泌铁载体,从组织、液体、细胞和蛋白质中提取Fe3+;革兰氏阴性细菌外膜的配基门控孔蛋白主动获取生成的铁载体,以及其他含铁分子,如血红素。相反,真核宿主通过将Fe3+隔离在结合蛋白和铁蛋白中来对抗细菌对铁的清除。革兰氏阴性细菌的铁摄取系统的多样性说明了促进微生物发病的一系列化学和生化机制。本文试图总结和理解这些过程,以指导发现可能阻止传染病的免疫或化学干预措施。
Iron is an indispensable metabolic cofactor in both pro- and eukaryotes, which engenders a natural competition for the metal between bacterial pathogens and their human or animal hosts. Bacteria secrete siderophores that extract Fe3+ from tissues, fluids, cells, and proteins; the ligand gated porins of the Gram-negative bacterial outer membrane actively acquire the resulting ferric siderophores, as well as other iron-containing molecules like heme. Conversely, eukaryotic hosts combat bacterial iron scavenging by sequestering Fe3+ in binding proteins and ferritin. The variety of iron uptake systems in Gram-negative bacterial pathogens illustrates a range of chemical and biochemical mechanisms that facilitate microbial pathogenesis. This document attempts to summarize and understand these processes, to guide discovery of immunological or chemical interventions that may thwart infectious disease.
Siderocalin/entobactin的相互作用:哺乳动物免疫与细菌铁转运之间的联系。
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