Iron is an essential nutrient for bacterial growth and is crucial for bacterial energy production, nucleotide synthesis, and regulation of gene expression. However, the availability of iron in a host is often limited by the tendency of iron to form complexes with iron binding proteins such as hemoglobin, transferrin, lactoferrin and ferritin, which cannot be used directly by bacteria. Therefore, to establish infection successfully in the human body, pathogenic bacteria require various iron acquisition mechanisms to obtain iron from host tissues. For example, microorganisms may obtain iron by invading host cells or by releasing siderophores, which are low-molecular-weight compounds with high affinity to chelate iron from iron-binding proteins. Additionally, a novel Isd iron acquisition system is present in Staphylococcus aureus.
Involvement of Iron in Biofilm Formation by Staphylococcus aureus. (2012) PLoS ONE 7(3): e34388. doi:10.1371/journal.pone.0034388
Staphylococcus aureus is a human pathogen that forms biofilm on catheters and medical implants. The authors’ earlier study established that 1,2,3,4,6-penta-O-galloyl-β-D-glucopyranose (PGG) inhibits biofilm formation by S. aureus by preventing the initial attachment of the cells to a solid surface and reducing the production of polysaccharide intercellular adhesin (PIA). Our cDNA microarray and MALDI-TOF mass spectrometric studies demonstrate that PGG treatment causes the expression of genes and proteins that are normally expressed under iron-limiting conditions. A chemical assay using ferrozine verifies that PGG is a strong iron chelator that depletes iron from the culture medium. This study finds that adding FeSO4 to a medium that contains PGG restores the biofilm formation and the production of PIA by S. aureus SA113. The requirement of iron for biofilm formation by S. aureus SA113 can also be verified using a semi-defined medium, BM, that contains an iron chelating agent, 2, 2′-dipyridyl (2-DP). Similar to the effect of PGG, the addition of 2-DP to BM medium inhibits biofilm formation and adding FeSO4 to BM medium that contains 2-DP restores biofilm formation. This study reveals an important mechanism of biofilm formation by S. aureus SA113.