Physical mechanisms driving the reversible aggregation of Staphylococcus aureus and response to antimicrobials

Abstract

Formation of non-sessile, auto-aggregated cells of Staphylococcus aureus contributes to surface colonization and biofilm formation, hence play a major role in the early establishment of infection and in tolerance to antimicrobials. Understanding the mechanism of aggregation and the impact of aggregation on the activity of antimicrobials is crucial in achieving a better control of this important pathogen. Previously linked to biological phenomena, physical interactions leading to S. aureus cellular aggregation and its protective features against antimicrobials remain unraveled. Herein, in-vitro experiments coupled with XDLVO simulations reveal that suspensions of S. aureus cells exhibit rapid, reversible aggregation (> 70%) in part controlled by the interplay between cellular hydrophobicity, surface potential and extracellular proteins. Changing pH and salt concentration in the extracellular media modulated the cellular surface potential but not the hydrophobicity which remained consistent despite these variations. A decrease in net cellular negative surface potential achieved by decreasing pH or increasing salt concentrations, caused attractive forces such as the hydrophobic and cell–protein interactions to prevail, favoring immediate aggregation. The aggregation significantly increased the tolerance of S. aureus cells to quaternary ammonium compounds (QAC). The well-dispersed cell population was completely inactivated within 30 s whereas its aggregated counterpart required more than 10 min.

Biofilm formation and inflammatory potential of Staphylococcus saccharolyticus: A possible cause of orthopedic implant-associated infections

“…Staphylococcal biofilms can form on the surface of implants or tissues, but they can also form as non-adherent multicellular aggregates ( Crosby et al, 2016 ; Otto, 2018 ; Schilcher and Horswill, 2020 ; Burel et al, 2021 ). Such aggregates have the same phenotypic properties as adherent biofilms in terms of immune evasion and antimicrobial tolerance.…”

Anti-Biofilm Potential of Nanonized Eugenol againstPseudomonas aeruginosa

“…The second step of biofilm establishment i.e., the micro-colony formation is characterized by bacterial adhesion, aggregation and persistence; each of these phenomena are dependent on cell surface hydrophobicity (CSH). Generally, P. aeruginosa exhibits hydrophobic cell surface, which is correlated with slow growth, strong biofilm formation and persistence (49); clinical isolates of mucoid, slime-producing strains of P. aeruginosa become non-adherent by alteration of CSH, while non-mucoid, non-slime producing strain become adherent with high affinity by increasing CSH (50). Eugenol is shown to inhibit biofilm formation and adhesion on Hep-2 (human larynx epidermoid carcinoma) cell line and on polystyrene by decreasing of CSH in Candida dubiliniensis and C. tropicalis (51).…”

Cellular Modifications of Rhodococci Exposed to Separate and Combined Effects of Pharmaceutical Pollutants

“…It allows for the cells' protection from toxic effects and their joint attack on a substrate for more effective degradation/transformation [41][42][43]. Auto-aggregation can be based on various physicochemical and molecular mechanisms [40,44]. An informative biophysical parameter of bacterial cells is their surface charge, dependent on biochemical composition of the cell surface (and a physiological state of cells) and evaluated by their electrokinetic potential (zeta potential).…”