Abstract

Silver, in the form of nanostructures, is widely employed as an antimicrobial agent. The origin of the biocidal mechanism has been elucidated in the last decades, originating from silver cation release due to oxidative dissolution followed by cellular uptake of silver ions, a process that causes a severe disruption of bacterial metabolism, leading to eradication. Despite the large body of work addressing the effects of nanosilver shape/size on the antibacterial mechanism and on the (bio)physical chemistry pathways that drive bacterial eradication, little effort has been devoted to the investigation of nanostructured silver plasmon response upon interaction with bacteria. We investigate the bacteria-induced changes of the plasmonic response of silver nanoplates after exposure to the bacterial model Escherichia coli. Ultrafast pump-probe measurements indicate that the dramatic changes on particle size/shape and crystallinity, which likely stem from a bacteria-induced oxidative dissolution process, translate into a clear modification of the plasmonic response. Specifically, exposure to bacteria causes a decrease in the electron–phonon coupling time and an increase in lattice-environment coupling time, effects explained by an increase in the free electron density and amorphization of the silver particles. Coherent oscillations that are observed in pristine silver are completely damped in contaminated samples, which can be attributed again to amorphization of the nanoplates at the surface and an increase in polydispersivity of particle geometries. This study opens innovative avenues in the biophysics of bio-responsive materials, with the aim of providing reliable biophysical signatures of the interaction of plasmonic materials with complex biological environments.

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