Staphylococcus aureus causes a significant amount of human morbidity and mortality. The ability of S. aureus to cause disease is dependent upon its acquisition of iron from the host. S. aureus can obtain iron from various sources during infection, including heme and transferrin. The most abundant iron source in humans is heme-iron bound by hemoglobin contained within erythrocytes. S. aureus is known to lyse erythrocytes through secretion of pore-forming toxins, providing access to host hemoglobin.

Proteins of the iron-regulated surface determinant (Isd) system bind host hemoproteins, remove the heme cofactor, and shuttle heme into the cytoplasm for use as a nutrient iron source. Deletion of Isd system components decreases staphylococcal virulence, underscoring the importance of heme-iron acquisition during infection. In addition to heme, S. aureus can utilize transferrin-iron through the secretion of siderophores. Several staphylococcal siderophores have been described, some of which have defined roles during the pathogenesis of staphylococcal infections. A greater understanding of staphylococcal iron acquisition may lead to the development of novel therapeutic strategies that target nutrient uptake and decrease the threat of this increasingly drug-resistant bacterial pathogen.

Further reading: Iron Uptake and Homeostasis in Microorganisms

Labels: Heme, Heme uptake, Iron acquisition mechanisms, Iron transporters, Iron uptake in Staphylococci, Iron uptake systems, Iron-homeostasis, Iron-uptake, Siderophore, Siderophores, Staphylococci