Iron and infection

被引:207
作者
Ganz, Tomas [1 ,2 ]
机构
[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, CHS 52-243,10833 Le Conte Ave, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol, CHS 52-243,10833 Le Conte Ave, Los Angeles, CA 90095 USA
关键词
Lipocalin; Lactoferrin; Hepcidin; Ferroportin; Nramp2; YERSINIA-ENTEROCOLITICA INFECTION; HEPCIDIN EXPRESSION; IFN-GAMMA; ANEMIA; PATHOGEN; LACTOFERRIN; PROTEIN; NRAMP1; HEMOCHROMATOSIS; HYPOFERREMIA;
D O I
10.1007/s12185-017-2366-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:7 / 15
页数:9
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