Nasal commensals reduce Staphylococcus aureus proliferation by restricting siderophore availability.

The human microbiome is critically associated with human health and disease. One aspect of this is that antibiotic-resistant opportunistic bacterial pathogens, such as methicillin-resistant Staphylococcus aureus, can reside within the nasal microbiota, which increases the risk of infection. Epidemiological studies of the nasal microbiome have revealed positive and negative correlations between non-pathogenic species and S.

Functional membrane microdomains and the hydroxamate siderophore transporter ATPase FhuC govern Isd-dependent heme acquisition in .

Sufficient access to transition metals such as iron is essential for bacterial proliferation and their active limitation within host tissues effectively restricts infection. To overcome iron limitation, the invasive pathogen uses the iron-regulated surface determinant (Isd) system to acquire hemoglobin-derived heme. While heme transport over the cell wall is well understood, its transport over the membrane is hardly investigated.

Nutritional Interactions between Bacterial Species Colonising the Human Nasal Cavity: Current Knowledge and Future Prospects.

The human nasal microbiome can be a reservoir for several pathogens, including . However, certain harmless nasal commensals can interfere with pathogen colonisation, an ability that could be exploited to prevent infection. Although attractive as a prophylactic strategy, manipulation of nasal microbiomes to prevent pathogen colonisation requires a better understanding of the molecular mechanisms of interaction that occur between nasal commensals as well as between commensals and pathogens.

In vivo growth of Staphylococcus lugdunensis is facilitated by the concerted function of heme and non-heme iron acquisition mechanisms.

Staphylococcus lugdunensis has increasingly been recognized as a pathogen that can cause serious infection indicating this bacterium overcomes host nutritional immunity. Despite this, there exists a significant knowledge gap regarding the iron acquisition mechanisms employed by S. lugdunensis, especially during infection of the mammalian host.