Ganz T
Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles 90095-1690, USA.
Curr Top Microbiol Immunol. 2006;306:183-98. doi: 10.1007/3-540-29916-5_7.
Hepcidin is a cationic amphipathic peptide made in the liver, released into plasma and excreted in urine. Hepcidin is the homeostatic regulator of intestinal iron absorption, iron recycling by macrophages, and iron mobilization from hepatic stores, but it is also markedly induced during infections and inflammation. Under the influence of hepcidin, macrophages, hepatocytes, and enterocytes retain iron that would otherwise be released into plasma. Hepcidin acts by inhibiting the efflux of iron through ferroportin, the sole known iron exporter that is expressed in the small intestine, and in hepatocytes and macrophages. As befits an iron-regulatory hormone, hepcidin synthesis is increased by iron loading, and decreased by anemia and hypoxia. Hepcidin is also rapidly induced by cytokines, including IL-6. The resulting decrease in plasma iron levels eventually limits iron availability to erythropoiesis and contributes to the anemia associated with infection and inflammation. The decrease in extracellular iron concentrations due to hepcidin probably limits iron availability to invading microorganisms, thus contributing to host defense.
铁调素是一种由肝脏产生的阳离子两亲性肽，释放到血浆中并经尿液排泄。铁调素是肠道铁吸收、巨噬细胞铁循环以及肝脏铁储备中铁动员的稳态调节因子，但在感染和炎症期间也会显著诱导产生。在铁调素的影响下，巨噬细胞、肝细胞和肠上皮细胞会保留原本会释放到血浆中的铁。铁调素通过抑制铁转运蛋白介导的铁外流发挥作用，铁转运蛋白是唯一已知的在小肠、肝细胞和巨噬细胞中表达的铁输出蛋白。作为一种铁调节激素，铁调素的合成在铁负荷增加时会增加，而在贫血和缺氧时会减少。铁调素也会被包括白细胞介素-6在内的细胞因子迅速诱导产生。血浆铁水平的降低最终会限制红细胞生成可利用的铁，并导致与感染和炎症相关的贫血。铁调素导致的细胞外铁浓度降低可能会限制入侵微生物可利用的铁，从而有助于宿主防御。
