Protein-based biofilm matrices in Staphylococci

Abstract

Staphylococcus aureus and Staphylococcus epidermidis are the most important etiological agents of biofilm associated-infections on indwelling medical devices. Biofilm infections may also develop independently of indwelling devices, e.g., in native valve endocarditis, bone tissue, and open wounds. After attachment to tissue or indwelling medical devices that have been conditioned with host plasma proteins, staphylococcal biofilms grow, and produce a specific environment which provides the conditions for cell–cell interaction and formation of multicellular communities. Bacteria living in biofilms express a variety of macromolecules, including exopolysaccharides, proteins, extracellular eDNA, and other polymers. The S. aureus surface protein C and G (SasC and SasG), clumping factor B (ClfB), serine aspartate repeat protein (SdrC), the biofilm-associated protein (Bap), and the fibronectin/fibrinogen-binding proteins (FnBPA and FnBPB) are individually implicated in biofilm matrix formation. In S. epidermidis, a protein named accumulation-associated protein (Aap) contributes to both the primary attachment phase and the establishment of intercellular connections by forming fibrils on the cell surface. In S. epidermidis, proteinaceous biofilm formation can also be mediated by the extracellular matrix binding protein (Embp) and S. epidermidis surface protein C (SesC). Additionally, multifunctional proteins such as extracellular adherence protein (Eap) and extracellular matrix protein binding protein (Emp) of S. aureus and the iron-regulated surface determinant protein C (IsdC) of S. lugdunensis can promote biofilm formation in iron-depleted conditions. This multitude of proteins intervene at different stages of biofilm formation with certain proteins contributing to biofilm accumulation and others mediating primary attachment to surfaces. This review examines the contribution of proteins to biofilm formation in Staphylococci. The potential to develop vaccines to prevent protein-dependent biofilm formation during staphylococcal infection is discussed.

Biofilm formation of Brazilian meticillin-resistant Staphylococcus aureus strains: prevalence of biofilm determinants and clonal profiles

“…The fibronectin-binding proteins, especially FnBPB, can mediate the attachment to tissue or synthetic surfaces of medical devices coated with plasma proteins, such as fibronectin (Vergara-Irigaray et al, 2009;Speziale et al, 2014). Once attached, staphylococcal biofilms grow by proliferation and production of a proteinaceous extracellular matrix.…”

MRSA and MSSA: The Mechanism of Methicillin Resistance and the Influence of Methicillin Resistance on Biofilm Phenotype of Staphylococcus aureus

“…Activation of agr system causes reduction in bioilm production due to the production of phenol-soluble modulins (PSMs) as surfactants, proteases, and nucleases that disperse microorganisms embedded in bioilm by enzymatic degradation of the bioilm matrix [14,21,22].…”

Molecular interactions and inhibition of the staphylococcal biofilm-forming protein SdrC

“…A variety of cell-surface components are involved in intercellular interactions (2,3). Although the polycationic polysaccharide intercellular adhesin has long been thought to be the main component promoting intercellular adhesion (4,5), there is now a compelling body of evidence that cell wall-anchored (CWA) proteins are also involved (2,3). Several recombinant CWA proteins have been shown to form dimers in solution (6)(7)(8)(9).…”

“…Biofilm formation is initiated by attachment of the bacteria to abiotic surfaces, protein-coated materials, and host cells, and followed by cell-cell adhesion and multiplication leading to a mature biofilm (1,2). A variety of cell-surface components are involved in intercellular interactions (2,3). Although the polycationic polysaccharide intercellular adhesin has long been thought to be the main component promoting intercellular adhesion (4,5), there is now a compelling body of evidence that cell wall-anchored (CWA) proteins are also involved (2,3).…”