Bovicin HC5 and nisin reduce Staphylococcus aureus adhesion to polystyrene and change the hydrophobicity profile and Gibbs free energy of adhesion

• Bovicin HC5 and nisin reduced adhesion of S. aureus to polystyrene surface.
• Both bacteriocins changed the hydrophobicity of cell and polystyrene surfaces.
• In the presence of the bacteriocins the free energy of adhesion was unfavorable.
• Bovicin HC5 and nisin changed biofilm-related gene expression in planktonic cells.

Staphylococcus aureus is an opportunistic pathogen often multidrug-resistant that not only causes a variety of human diseases, but also is able to survive on biotic and abiotic surfaces through biofilm communities. The best way to inhibit biofilm establishment is to prevent cell adhesion. In the present study, subinhibitory concentrations of the bacteriocins bovicin HC5 and nisin were tested for their capability to interfere with the adhesion of S. aureus to polystyrene. Subinhibitory dosages of the bacteriocins reduced cell adhesion and this occurred probably due to changes in the hydrophobicity of the bacterial cell and polystyrene surfaces. After treatment with bovicin HC5 and nisin, the surfaces became more hydrophilic and the free energy of adhesion (∆Gadhesion) between bacteria and the polystyrene surface was unfavorable. The transcriptional level of selected genes was assessed by RT-qPCR approach, revealing that the bacteriocins affected the expression of some important biofilm associated genes (icaD, fnbA, and clfB) and rnaIII, which is involved in the quorum sensing mechanism. The conditioning of food-contact surfaces with bacteriocins can be an innovative and powerful strategy to prevent biofilms in the food industry. The results are relevant for food safety as they indicate that bovicin HC5 and nisin can inhibit bacterial adhesion and consequent biofilm establishment, since cell adhesion precedes biofilm formation.