Relevant role of fibronectin-binding proteins in Staphylococcus aureus biofilm-associated foreign-body infections.
Staphylococcus aureus can establish chronic infections on implanted medical devices due to its capacity to form biofilms. Analysis of the factors that assemble cells into a biofilm has revealed the occurrence of strains that produce either a polysaccharide intercellular adhesin/poly-N-acetylglucosamine (PIA/PNAG) exopolysaccharide- or a protein-dependent biofilm. Examination of the influence of matrix nature on the biofilm capacities of embedded bacteria has remained elusive, because a natural strain that readily converts between a polysaccharide- and a protein-based biofilm has not been studied. Here, we have investigated the clinical methicillin (meticillin)-resistant Staphylococcus aureus strain 132, which is able to alternate between a proteinaceous and an exopolysaccharidic biofilm matrix, depending on environmental conditions. Systematic disruption of each member of the LPXTG surface protein family identified fibronectin-binding proteins (FnBPs) as components of a proteinaceous biofilm formed in Trypticase soy broth-glucose, whereas a PIA/PNAG-dependent biofilm was produced under osmotic stress conditions. The induction of FnBP levels due to a spontaneous agr deficiency present in strain 132 and the activation of a LexA-dependent SOS response or FnBP overexpression from a multicopy plasmid enhanced biofilm development, suggesting a direct relationship between the FnBP levels and the strength of the multicellular phenotype. Scanning electron microscopy revealed that cells growing in the FnBP-mediated biofilm formed highly dense aggregates without any detectable extracellular matrix, whereas cells in a PIA/PNAG-dependent biofilm were embedded in an abundant extracellular material. Finally, studies of the contribution of each type of biofilm matrix to subcutaneous catheter colonization revealed that an FnBP mutant displayed a significantly lower capacity to develop biofilm on implanted catheters than the isogenic PIA/PNAG-deficient mutant.
Vergara-Irigaray
Marta
M
Laboratory of Microbial Biofilms, Instituto de Agrobiotecnología, Universidad Pública de Navarra-CSIC-Gobierno de Navarra, 31006 Pamplona, Spain.
Valle
Jaione
J
Merino
Nekane
N
Latasa
Cristina
C
García
Begoña
B
Ruiz de Los Mozos
Igor
I
Solano
Cristina
C
Toledo-Arana
Alejandro
A
Penadés
José R
JR
Lasa
Iñigo
I
D000117:Acetylglucosamine / Q000502:physiology; D018829:Adhesins, Bacterial / Q000502:physiology*; D001426:Bacterial Proteins / Q000502:physiology; D018441:Biofilms; D055499:Catheter-Related Infections / Q000209:etiology*; D006801:Humans; D011135:Polysaccharides, Bacterial / Q000502:physiology; D013014:SOS Response, Genetics; D013203:Staphylococcal Infections / Q000209:etiology*; D013211:Staphylococcus aureus / Q000502:physiology*; D015534:Trans-Activators / Q000502:physiology
D018829:Adhesins, Bacterial; C095698:Agr protein, Staphylococcus aureus; D001426:Bacterial Proteins; D011135:Polysaccharides, Bacterial; D015534:Trans-Activators; C078635:fibronectin-binding proteins, bacterial; C113831:poly-N-acetyl glucosamine; C113579:polysaccharide intercellular adhesin; D000117:Acetylglucosamine