Nairz Manfred, Weiss Günter
Department of Internal Medicine II, Infectious Diseases, Immunology, Rheumatology, Pneumology, Medical University of Innsbruck, Austria.
Department of Internal Medicine II, Infectious Diseases, Immunology, Rheumatology, Pneumology, Medical University of Innsbruck, Austria; Christian Doppler Laboratory for Iron Metabolism and Anemia Research, Medical University of Innsbruck, Austria.
Mol Aspects Med. 2020 Oct;75:100864. doi: 10.1016/j.mam.2020.100864. Epub 2020 May 24.
Iron is an essential micronutrient for virtually all living cells. In infectious diseases, both invading pathogens and mammalian cells including those of the immune system require iron to sustain their function, metabolism and proliferation. On the one hand, microbial iron uptake is linked to the virulence of most human pathogens. On the other hand, the sequestration of iron from bacteria and other microorganisms is an efficient strategy of host defense in line with the principles of 'nutritional immunity'. In an acute infection, host-driven iron withdrawal inhibits the growth of pathogens. Chronic immune activation due to persistent infection, autoimmune disease or malignancy however, sequesters iron not only from infectious agents, autoreactive lymphocytes and neoplastic cells but also from erythroid progenitors. This is one of the key mechanisms which collectively result in the anemia of chronic inflammation. In this review, we highlight the most important interconnections between iron metabolism and immunity, focusing on host defense against relevant infections and on the clinical consequences of anemia of inflammation.
铁是几乎所有活细胞必需的微量营养素。在传染病中，入侵的病原体和包括免疫系统细胞在内的哺乳动物细胞都需要铁来维持其功能、代谢和增殖。一方面，微生物对铁的摄取与大多数人类病原体的毒力有关。另一方面，从细菌和其他微生物中螯合铁是一种符合“营养免疫”原则的有效宿主防御策略。在急性感染中，宿主驱动的铁撤离会抑制病原体的生长。然而，由于持续感染、自身免疫性疾病或恶性肿瘤导致的慢性免疫激活，不仅会从感染因子、自身反应性淋巴细胞和肿瘤细胞中螯合铁，还会从红系祖细胞中螯合铁。这是导致慢性炎症性贫血的关键机制之一。在这篇综述中，我们强调了铁代谢与免疫之间最重要的相互联系，重点关注宿主对相关感染的防御以及炎症性贫血的临床后果。
