Hepcidin--a peptide hormone at the interface of innate immunity and iron metabolism.
Hepcidin--a peptide hormone at the interface of innate immunity and iron metabolism.
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DOI：
10.1007/3-540-29916-5_7
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发表时间：
2006
影响因子：
--
通讯作者：
T. Ganz
中科院分区：
文献类型：
--
作者：
T. Ganz
铁调素是一种阳离子两亲性肽，在肝脏中产生，释放到血浆中并经尿液排泄。铁调素是肠铁吸收、巨噬细胞铁再循环和肝脏储存铁动员的稳态调节剂，但它在感染和炎症期间也被显著诱导。在铁调素的影响下，巨噬细胞、肝细胞和肠细胞保留铁，否则铁将被释放到血浆中。铁调素通过抑制铁通过膜铁转运蛋白（ferroportin）的流出而起作用，膜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。铁调素作为一种铁调节激素，铁调素的合成随着铁负荷的增加而增加，随着贫血和缺氧而减少。铁调素也被细胞因子（包括IL-6）快速诱导。血浆铁水平的降低最终限制了红细胞生成的铁可用性，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的降低可能限制了入侵微生物的铁可用性，从而有助于宿主防御。
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.