How acesulfame-K affected drug-resistant bacteria and antibiotic activity.

What is it about?

In this study, we screened a panel of artificial sweeteners against multidrug-resistant bacteria and found that several inhibited growth, with acesulfame-K (ace-K) showing a strong and consistent effect that we then studied in detail. Using Acinetobacter baumannii as our main model, alongside Pseudomonas aeruginosa and other clinically relevant bacterial isolates, we found that ace-K could slow bacterial growth, reduce biofilm formation, impair surface movement and block natural transformation, a route by which bacteria can acquire new genes. Gene expression and microscopy experiments suggested that ace-K disrupts the bacterial outer cell layers and membrane, making cells more permeable and leading to membrane bulging and cell lysis. We also found that, at non-lethal concentrations, ace-K could make multidrug-resistant A. baumannii more sensitive to several antibiotics, including carbapenems, and that its antimicrobial activity was maintained in an ex vivo porcine skin wound model.

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Photo by Towfiqu barbhuiya on Unsplash

Photo by Towfiqu barbhuiya on Unsplash

Why is it important?

This matters because antimicrobial resistance is made worse by behaviours such as biofilm formation, spread across surfaces and the acquisition of resistance genes, all of which can make infections harder to treat. Our findings suggest that ace-K may be useful not only because it can inhibit some pathogens directly, but also because it can weaken traits linked to persistence and improve the activity of existing antibiotics against a resistant strain. The wound-model results further support exploring whether ace-K could contribute to topical or combination approaches, while also showing that familiar dietary compounds may be a useful source of antimicrobial leads.