The significance of extracellular DNA (eDNA) in biofilms was overlooked until researchers added DNAse to a Pseudomonas aeruginosa biofilm and watched the biofilm disappear. Now, a decade later, the widespread importance of eDNA in biofilm formation is undisputed, but detailed knowledge about how it promotes biofilm formation and conveys antimicrobial resistance is only just starting to emerge. In this review, we discuss how eDNA is produced, how it aids bacterial adhesion, secures the structural stability of biofilms and contributes to antimicrobial resistance. The appearance of eDNA in biofilms is no accident: It is produced by active secretion or controlled cell lysis - sometimes linked to competence development. eDNA adsorbs to and extends from the cell surface, promoting adhesion to abiotic surfaces through acid-base interactions. In the biofilm, is it less clear how eDNA interacts with cells and matrix components. A few eDNA-binding biomolecules have been identified, revealing new concepts in biofilm formation. Being anionic, eDNA chelates cations and restricts diffusion of cationic antimicrobials. Furthermore, chelation of Mg(2+) triggers a genetic response that further increases resistance. The multifaceted role of eDNA makes it an attractive target to sensitize biofilms to conventional antimicrobial treatment or development of new strategies to combat biofilms.

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We used hairy nanocrystalline cellulose functionalized with aldehyde groups, otherwise known as sterically stabilized nanocrystalline cellulose (SNCC), to facilitate the attachment of the antibacterial agents lysozyme and nisin. Immobilization was achieved using a simple, green process that does not require any linker or activator. X-ray photoelectron spectroscopy and Fourier transform infrared spectroscopy analyses showed successful attachment of both nisin and lysozyme onto the SNCC. The efficacy of the conjugated nanocellulose against the model bacteria Bacillus subtilis and Staphylococcus aureus was tested in terms of bacterial growth, cell viability, and biofilm formation/removal. The results show that the minimum inhibitory concentration of the conjugated nanocellulose is higher than that of lysozyme and nisin in free form, which was expected given that immobilization reduces the possible spatial orientations of these proteins. We observed that free nisin is not active against S. aureus after 24 h of exposure due to either deactivation of free nisin or development of resistance in S. aureus against free nisin. Interestingly, we did not observe this phenomenon when the bacteria were exposed to antibacterials immobilized on nanocellulose, suggesting that immobilization of antibacterial agents onto SNCC effectively retains their activity over long time periods. We suggest that antibacterial SNCC is a promising candidate for the development of antibacterial wound dressings.

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Antibiotic resistance is spreading at an alarming rate among pathogenic bacteria in both medicine and agriculture. Interfering with the intrinsic resistance mechanisms displayed by pathogenic bacteria has the potential to make antibiotics more effective and decrease the spread of acquired antibiotic resistance. Here, it is demonstrated that cranberry proanthocyanidin (cPAC) prevents the evolution of resistance to tetracycline in Escherichia coli and Pseudomonas aeruginosa , rescues antibiotic efficacy against antibiotic‐exposed cells, and represses biofilm formation. It is shown that cPAC has a potentiating effect, both in vitro and in vivo, on a broad range of antibiotic classes against pathogenic E. coli , Proteus mirabilis , and P. aeruginosa . Evidence that cPAC acts by repressing two antibiotic resistance mechanisms, selective membrane permeability and multidrug efflux pumps, is presented. Failure of cPAC to potentiate antibiotics against efflux pump‐defective mutants demonstrates that efflux interference is essential for potentiation. The use of cPAC to potentiate antibiotics and mitigate the development of resistance could improve treatment outcomes and help combat the growing threat of antibiotic resistance.