Staphylococcus aureus extracellular vesicles (EVs): surface-binding antagonists of biofilm formation.

The prevalence of Staphylococcus aureus worldwide as a nosocomial infectious agent is recognized but the reason behind the spread of this bacterium has remained elusive. Here, we hypothesized that the communication of S. aureus might benefit from it blocking other bacteria from establishing themselves on the surface. This was found to be the case for several pathogens as the S. aureus supernatant curtailed their ability to form biofilms. Subsequent analyses using Acinetobacter baumannii as a model found this effect is primarily mediated by S. aureus' extracellular vesicles (EVs), which bound to the polystyrene surface. We found the EV-treated surfaces were significantly more hydrophilic after EV treatment, a condition that made it difficult for A. baumannii to initially adhere to the polystyrene surface and reduced its resulting biofilm by up to 93%. Subsequent tests found this also extended to several other bacterial pathogens, with a 40-70% decrease in their biofilm mass. The S. aureus EVs and their activity still remained after the surface was washed with 10% bleach, while the use of ethylenediaminetetraacetic acid (EDTA) removed both the EVs from the surface and their activity.