Michels Kathryn, Nemeth Elizabeta, Ganz Tomas, Mehrad Borna
Departments of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, Virginia, United States of America.
Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, United States of America.
PLoS Pathog. 2015 Aug 20;11(8):e1004998. doi: 10.1371/journal.ppat.1004998. eCollection 2015 Aug.
Hepcidin is the master regulator of iron homeostasis in vertebrates. The synthesis of hepcidin is induced by systemic iron levels and by inflammatory stimuli. While the role of hepcidin in iron regulation is well established, its contribution to host defense is emerging as complex and multifaceted. In this review, we summarize the literature on the role of hepcidin as a mediator of antimicrobial immunity. Hepcidin induction during infection causes depletion of extracellular iron, which is thought to be a general defense mechanism against many infections by withholding iron from invading pathogens. Conversely, by promoting iron sequestration in macrophages, hepcidin may be detrimental to cellular defense against certain intracellular infections, although critical in vivo studies are needed to confirm this concept. It is not yet clear whether hepcidin exerts any iron-independent effects on host defenses.
铁调素是脊椎动物铁稳态的主要调节因子。铁调素的合成受全身铁水平和炎症刺激的诱导。虽然铁调素在铁调节中的作用已得到充分证实，但其在宿主防御中的作用正呈现出复杂多面的特点。在本综述中，我们总结了关于铁调素作为抗菌免疫介质作用的文献。感染期间铁调素的诱导会导致细胞外铁的消耗，这被认为是通过阻止入侵病原体获取铁来抵御多种感染的一种普遍防御机制。相反，通过促进巨噬细胞中的铁螯合，铁调素可能对细胞抵御某些细胞内感染有害，不过还需要关键的体内研究来证实这一概念。铁调素是否对宿主防御发挥任何与铁无关的作用尚不清楚。
