About this Research Topic
Macrophages play an important role in host defense against invading bacterial pathogens and a central role in iron homeostasis since they engulf senescent red blood cells and recycle iron for erythropoiesis. In response to infection the host limits the bioavailability of iron by up-regulating expression of hepcidin, the master iron-regulating hormone, which limits iron uptake from the gut and retains iron in macrophages. The host also limits the egress of iron from macrophages by down-regulating expression of ferroportin, the only known cellular iron exporter. Therefore, iron-limiting innate immune response via the hepcidin-ferroportin axis results in a transient hypoferremia known as anemia of infection. Retaining iron in macrophages if prolonged can cause iron misdistribution which is known as anemia of chronic disease. This altered iron homeostasis is associated with many chronic inflammatory and degenerative diseases.
This Research Topic will cover the strategies used by different pathogens to acquire iron, including Gram-positive bacteria (Mycobacterium and Staphylococcus aureus), Gram-negative (E. coli, Pseudomonas aeruginosa, Haemophilus influenzae, Bordetella pertussis, Yersinia pestis, Burkholderia cenocepacia, Francisella tullarensis, Neisseria meningitidis, Vibrio) and one pathogenic fungus (Candida). The Research Topic will also cover the host strategies to limit iron bioavailability and the consequent pathophysiological responses. Research articles as well as short reviews will be accepted as contributions.
Keywords: Iron, siderophores, transferrin, lactoferrin, heme, ferrous iron uptake.
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