About this Research Topic
For most microorganisms iron is an essential element since it is involved in many reactions in the cell. It is involved in oxido-reduction mechanisms involving heme-containing proteins, such as cytochromes. It is also present in Fe S proteins involved in essential enzymatic reactions. Iron is an abundant element, but it is not always available. Fe3+ under aerobic conditions is not soluble while Fe2+ is soluble under anaerobic condition. Pathogenic microorganism such as bacteria and fungi are confronted with the problem of iron sequestration by lactoferrin in secretions and transferrin in blood while the remaining iron is intracellular in hemoproteins or associated with proteins such as ferritins. Pathogens have devised different strategies to acquire iron, by the use of high-affinity siderophores, by taking up heme from hemoproteins, by using Fe2+ iron uptake systems under anaerobic conditions, or by taking up iron directly from transferrin and lactoferrin.
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.
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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