Iron and infection
Iron and infection
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DOI：
10.1007/s12185-017-2366-2
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发表时间：
2018-01-01
影响因子：
2.1
通讯作者：
Ganz, Tomas
中科院分区：
文献类型：
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作者：
Ganz, Tomas
铁是几乎所有具有感染性的微生物必需的微量金属，宿主防御机制针对这种依赖来剥夺微生物的铁。这篇综述强调了在感染过程中被激活的机制，以限制粘膜表面、血浆和细胞外液以及巨噬细胞内的铁。铁超载疾病，如遗传性血色素沉着症或β-地中海贫血，干扰限制铁的宿主反应，从而导致更容易受到利用这种脆弱性的微生物的感染。炎症性贫血(以前称为慢性病贫血)是一种宿主防御的非靶点效应，其中炎性细胞因子通过激活巨噬细胞缩短红细胞寿命，优先在骨髓中产生白细胞，并诱导海普西丁增加血浆转铁蛋白饱和度和非转铁蛋白结合铁的浓度。
Iron is an essential trace metal for nearly all infectious microorganisms, and host defense mechanisms target this dependence to deprive microbes of iron. This review highlights mechanisms that are activated during infections to restrict iron on mucosal surfaces, in plasma and extracellular fluid, and within macrophages. Iron overload disorders, such as hereditary hemochromatosis or beta-thalassemia, interfere with iron-restrictive host responses, and thereby cause increased susceptibility to infections with microbes that can exploit this vulnerability. Anemia of inflammation (formerly known as anemia of chronic diseases) is an "off-target" effect of host defense wherein inflammatory cytokines shorten erythrocyte lifespan by activating macrophages, prioritize leukocyte production in the marrow, and induce hepcidin to increase plasma transferrin saturation and the concentration of non-transferrin-bound iron.