A NovelStaphylococcus aureusBiofilm Phenotype Mediated by the Fibronectin-Binding Proteins, FnBPA and FnBPB

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Abstract
Device-associated infections involving biofilm remain a persistent clinical problem. We recently reported that four methicillin-resistantStaphylococcus aureus(MRSA) strains formed biofilm independently of theicaADBC-encoded exopolysaccharide. Here, we report that MRSA biofilm development was promoted under mildly acidic growth conditions triggered by the addition of glucose to the growth medium. Loss of sortase, which anchors LPXTG-containing proteins to peptidoglycan, reduced the MRSA biofilm phenotype. Furthermore introduction of mutations infnbAandfnbB, which encode the LPXTG-anchored multifunctional fibrinogen and fibronectin-binding proteins, FnBPA and FnBPB, reduced biofilm formation by several MRSA strains. However, these mutations had no effect on biofilm formation by methicillin-sensitiveS. aureusstrains. FnBP-promoted biofilm occurred at the level of intercellular accumulation and not primary attachment. Mutation offnbAorfnbBalone did not substantially affect biofilm, and expression of either gene alone from a complementing plasmid infnbA fnbBmutants restored biofilm formation. FnBP-promoted biofilm was dependent on the integrity of SarA but not through effects onfnbAorfnbBtranscription. Using plasmid constructs lacking regions of FnBPA to complement anfnbABmutant revealed that the A domain alone and not the domain required for fibronectin binding could promote biofilm. Additionally, an A-domain N304A substitution that abolished fibrinogen binding did not affect biofilm. These data identify a novelS. aureusbiofilm phenotype promoted by FnBPA and FnBPB which is apparently independent of the known ligand-binding activities of these multifunctional surface proteins.