Abstract
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.
Highlights
Staphylococcus aureus is an opportunistic pathogen, which forms biofilms on medical devices and causes pneumonia, meningitis, endocarditis, osteomyelitis and septicemia [1]
Our earlier work showed that PGG inhibits biofilm formation by S. aureus SA113 [25], this study examined further how PGG affects the expression of these surface proteins
Our cDNA microarray analysis using RNA isolated from S. aureus SA113 that had been cultured in TSBg-PGG medium found that PGG treatment caused transcription of genes that are expressed under iron-limiting conditions, including those genes encoding the synthesis of siderophores, iron ABC transporter proteins, FeoB-family ferrous iron uptake proteins, and IsdA (Table S1), suggesting that PGG depletes iron from the culturing medium
Summary
Staphylococcus aureus is an opportunistic pathogen, which forms biofilms on medical devices and causes pneumonia, meningitis, endocarditis, osteomyelitis and septicemia [1]. The formation of a biofilm involves the attachment and accumulation of bacterial cells within a slimy substance on a solid surface [2]. The biofilm formation by S. aureus involves complex processes. The expression of the ica operon and subsequent biofilm formation is strongly influenced by a variety of external conditions, including nutrient supply, osmolarity, temperature and sub-inhibitory concentrations of certain antibiotics [6]. Ica-independent mechanisms of biofilm formation by S. aureus have been reported [7]. Other surface proteins of S. aureus that contribute to adherence and biofilm formation include fibronectin-binding proteins A and B (FnBPA and FnBPB) [8], the collagen-binding protein Cna [9], and the fibrinogen-binding proteins, clumping factors A and B (ClfA and ClfB) [10]
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