Molecular mechanisms of Staphylococcus aureus iron acquisition

Heme Iron is required for Staphylococcus aureus growth and persistence and hence must be acquired during infection. Most vertebrate iron is utilized as a cofactor in biochemical reactions that occur intracellularly. This intracellular pool of iron is generally not available to extracellular pathogens such as S. aureus. Moreover, the amount of free iron found within the serum is negligible, as it is usually complexed to high-affinity iron-binding proteins. This process of iron sequestration by the host, also referred to as nutritional immunity, inhibits the growth of invading microorganisms. In response to this severe iron limitation, S. aureus has evolved sophisticated strategies to obtain iron required to proliferate within vertebrates. This review provides a comprehensive analysis of the pathways S. aureus utilizes to obtain iron during infection.

 

Molecular Mechanisms of Staphylococcus aureus Iron Acquisition. Annual Review of Microbiology June 2, 2011 doi: 10.1146/annurev-micro-090110-102851
The unique redox potential of iron is an ideal cofactor in diverse biochemical reactions. Iron is therefore vital for the growth and proliferation of nearly all organisms, including pathogenic bacteria. Vertebrates sequester excess iron within proteins in order to alleviate toxicity and restrict the amount of free iron available for invading pathogens. Restricting the growth of infectious microorganisms by sequestering essential nutrients is referred to as nutritional immunity. In order to circumvent nutritional immunity, bacterial pathogens have evolved elegant systems that allow for the acquisition of iron during infection. The gram-positive extracellular pathogen Staphylococcus aureus is a commensal organism that can cause severe disease when it gains access to underlying tissues. Iron acquisition is required for S. aureus colonization and subsequent pathogenesis. Herein we review the strategies S. aureus employs to obtain iron through the production of siderophores and the consumption of host heme.

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