Different binding mechanisms of Staphylococcus aureus to hydrophobic and hydrophilic surfaces.

Bacterial adhesion to surfaces is a crucial step in initial biofilm formation. In a combined experimental and computational approach, we studied the adhesion of the pathogenic bacterium Staphylococcus aureus to hydrophilic and hydrophobic surfaces. We used atomic force microscopy-based single-cell force spectroscopy and Monte Carlo simulations to investigate the similarities and differences of adhesion to hydrophilic and hydrophobic surfaces. Our results reveal that binding to both types of surfaces is mediated by thermally fluctuating cell wall macromolecules that behave differently on each type of substrate: on hydrophobic surfaces, many macromolecules are involved in adhesion, yet only weakly tethered, leading to high variance between individual bacteria, but low variance between repetitions with the same bacterium. On hydrophilic surfaces, however, only few macromolecules tether strongly to the surface. Since during every repetition with the same bacterium different macromolecules bind, we observe a comparable variance between repetitions and different bacteria. We expect these findings to be of importance for the understanding of the adhesion behaviour of many bacterial species as well as other microorganisms and even nanoparticles with soft, macromolecular coatings, used e.g. for biological diagnostics.

Stochastic binding of Staphylococcus aureus to hydrophobic surfaces.

The adhesion of pathogenic bacteria to surfaces is of immense importance for health care applications. Via a combined experimental and computational approach, we studied the initiation of contact in the adhesion process of the pathogenic bacterium Staphylococcus aureus. AFM force spectroscopy with single cell bacterial probes paired with Monte Carlo simulations enabled an unprecedented molecular investigation of the contact formation. Our results reveal that bacteria attach to a surface over distances far beyond the range of classical surface forces via stochastic binding of thermally fluctuating cell wall proteins. Thereby, the bacteria are pulled into close contact with the surface as consecutive proteins of different stiffnesses attach. This mechanism greatly enhances the attachment capability of S. aureus. It, however, can be manipulated by enzymatically/chemically modifying the cell wall proteins to block their consecutive binding. Our study furthermore reveals that fluctuations in protein density and structure are much more relevant than the exact form of the binding potential.