Publications by authors named "Vera Carniello"

Antimicrobials with nonselective antibacterial efficacy such as chlorhexidine can be effective in reducing biofilm, but bear the risk of inducing resistance in specific bacteria. In clinical practice, bacteria such as have been found resistant to chlorhexidine, but other bacteria, including , have largely remained susceptible to chlorhexidine despite its widespread use in oral healthcare. Here, we aim to forward a possible reason as to why can acquire resistance against chlorhexidine, while remains susceptible to chlorhexidine.

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Mechanosensitive channels in bacterial membranes open or close in response to environmental changes to allow transmembrane transport, including antibiotic uptake and solute efflux. In this paper, we hypothesize that gating of mechanosensitive channels is stimulated by forces through which bacteria adhere to surfaces. Hereto, channel gating is related with adhesion forces to different surfaces of a Staphylococcus aureus strain and its isogenic ΔmscL mutant, deficient in MscL (large) channel gating.

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Biofilm formation is initiated by adhesion of individual bacteria to a surface. However, surface adhesion alone is not sufficient to form the complex community architecture of a biofilm. Surface-sensing creates bacterial awareness of their adhering state on the surface and is essential to initiate the phenotypic and genotypic changes that characterize the transition from initial bacterial adhesion to a biofilm.

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In infections, bacteria often adhere to surfaces and become deformed by the forces with which they adhere. Nanoscopic cell wall deformation defines bacterial responses to environmental conditions and is likely influenced by antibiotics. Here, staphylococcal cell wall deformation upon exposure to cell wall active and non-active antibiotics or their combinations is compared for two green-fluorescent (GFP) isogenic Staphylococcus aureus strains adhering to a gold surface, of which one lacks peptidoglycan cross-linking.

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Unlabelled: Nisin-associated-sensitivity-response-regulator (NsaRS) in Staphylococcus aureus is important for its adhesion to surfaces and resistance against antibiotics, like nisin. NsaRS consists of an intra-membrane-located sensor NsaS and a cytoplasmatically-located response-regulator NsaR, which becomes activated upon receiving phosphate groups from the intra-membrane-located sensor.

Hypothesis: The intra-membrane location of the NsaS sensor leads us to hypothesize that the two-component NsaRS system not only senses "chemical" (nisin) but also "mechanical" (adhesion) stresses to modulate efflux of antibiotics from the cytoplasm.

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