Adhesion of bacteria occurs on virtually all natural and synthetic surfaces and is crucial for their survival. Once they are adhering, bacteria start growing and form a biofilm, in which they are protected against environmental attacks. Bacterial adhesion to surfaces is mediated by a combination of different short-and long-range forces. Here we present a new atomic force microscopy (AFM)-based method to derive long-range bacterial adhesion forces from the dependence of bacterial adhesion forces on the loading force, as applied during the use of AFM. The long-range adhesion forces of wild-type Staphylococcus aureus parent strains (0.5 and 0.8 nN) amounted to only one-third of these forces measured for their more deformable isogenic ⌬pbp4 mutants that were deficient in peptidoglycan cross-linking. The measured long-range Lifshitz-Van der Waals adhesion forces matched those calculated from published Hamaker constants, provided that a 40% ellipsoidal deformation of the bacterial cell wall was assumed for the ⌬pbp4 mutants. Direct imaging of adhering staphylococci using the AFM peak force-quantitative nanomechanical property mapping imaging mode confirmed a height reduction due to deformation in the ⌬pbp4 mutants of 100 to 200 nm. Across naturally occurring bacterial strains, long-range forces do not vary to the extent observed here for the ⌬pbp4 mutants. Importantly, however, extrapolating from the results of this study, it can be concluded that long-range bacterial adhesion forces are determined not only by the composition and structure of the bacterial cell surface but also by a hitherto neglected, small deformation of the bacterial cell wall, facilitating an increase in contact area and, therewith, in adhesion force. Bacteria adhere to virtually all natural and synthetic surfaces (1, 2), as adhesion is crucial for their survival. Bacterial adhesion to surfaces is followed by their growth and constitutes the first step in the formation of a biofilm, in which organisms are protected against antimicrobial treatment and environmental attacks. Accordingly, the biofilm mode of growth is highly persistent and biofilms are notoriously hard to remove, causing major problems in many industrial and biomedical applications, with high associated costs. On the other hand, biofilms can be beneficial, too, as in the bioremediation of soil, for instance. Surface thermodynamics and (extended) DLVO (Derjaguin and Landau, Verwey, and Overbeek) approaches have been amply applied in current microbiology to outline that bacterial adhesion to surfaces is mediated by an interplay of different fundamental physicochemical interactions, including Lifshitz-Van der Waals, electric double-layer, and acid-base forces (3-5). Assorted according to their different effective ranges, these different fundamental interactions can be alternatively categorized into two groups, short-range and long-range forces (6), that act over distances of a few nm up to 10s of nm, respectively.Long-range adhesion forces are generally associated with Lifshitz-Van der ...
The majority of human infections are caused by biofilms. The biofilm mode of growth enhances the pathogenicity of Staphylococcus spp. considerably, because once they adhere, staphylococci embed themselves in a protective, self-produced matrix of extracellular polymeric substances (EPSs). The aim of this study was to investigate the influence of forces of staphylococcal adhesion to different biomaterials on icaA (which regulates the production of EPS matrix components) and cidA (which is associated with cell lysis and extracellular DNA [eDNA] release) gene expression in Staphylococcus aureus biofilms. Experiments were performed with S. aureus ATCC 12600 and its isogenic mutant, S. aureus ATCC 12600 ⌬pbp4, deficient in peptidoglycan cross-linking. Deletion of pbp4 was associated with greater cell wall deformability, while it did not affect the planktonic growth rate, biofilm formation, cell surface hydrophobicity, or zeta potential of the strains. The adhesion forces of S. aureus ATCC 12600 were the strongest on polyethylene (4.9 ؎ 0.5 nN), intermediate on polymethylmethacrylate (3.1 ؎ 0.7 nN), and the weakest on stainless steel (1.3 ؎ 0.2 nN). The production of poly-N-acetylglucosamine, eDNA presence, and expression of icaA genes decreased with increasing adhesion forces. However, no relation between adhesion forces and cidA expression was observed. The adhesion forces of the isogenic mutant S. aureus ATCC 12600 ⌬pbp4 (deficient in peptidoglycan cross-linking) were much weaker than those of the parent strain and did not show any correlation with the production of poly-N-acetylglucosamine, eDNA presence, or expression of the icaA and cidA genes. This suggests that adhesion forces modulate the production of the matrix molecule poly-N-acetylglucosamine, eDNA presence, and icaA gene expression by inducing nanoscale cell wall deformation, with cross-linked peptidoglycan layers playing a pivotal role in this adhesion force sensing. Staphylococcus spp. present an important group of potentially pathogenic strains and species. According to estimates by the National Institutes of Health, about 80% of all human infections are caused by biofilms (1). The biofilm mode of growth considerably enhances the pathogenicity of Staphylococcus spp. when the biofilm is formed on the surfaces of biomaterial implants and devices, such as total knee or hip arthroplasties or pacemakers (2). Biofilm formation starts with the adhesion of individual organisms to a substratum surface. Initially, adhesion is reversible, but the bond between an adhering organism and a substratum surface rapidly matures over time to become stronger, and eventually, adhesion is irreversible (3). Adhesion is further enforced through the production of a matrix consisting of extracellular polymeric substances (EPSs) by the adhering organisms, in which they grow and find shelter against the host immune system and antibiotic treatment. The EPS composition largely depends on the bacterial strains and environmental conditions, but major components of EPSs across differen...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.