Sweetener specific modulation of physiological responses in uropathogenic Escherichia coli

Artificial and non-nutritive sweeteners are increasingly consumed worldwide, yet their effects on bacterial pathogens remain poorly understood. Here, we investigated the impact of the artificial sweetener acesulfame potassium (ace-K) and natural non-nutritive sweetener stevia on clinically relevant uropathogenic Escherichia coli isolates previously identified in the Norfolk region. Comparative phenotypic analyses revealed strain-specific responses to sweetener exposure, with the clinical isolate GL204 demonstrating marked responsiveness to both compounds. Transcriptomic analysis of GL204 following exposure to ace-K or stevia identified distinct adaptive responses, with stevia predominantly inducing genes associated with metabolic pathways, whereas ace-K significantly upregulated genes involved in bacterial motility. These transcriptional changes were supported by phenotypic assays, demonstrating that ace-K significantly enhanced bacterial motility, while stevia supported bacterial growth as a usable carbon source in GL204. Together, these findings demonstrate that chemically-distinct sweeteners differentially modulate key pathogenic traits in a uropathogenic E. coli strain through discrete physiological mechanisms. The ability of ace-K to promote motility and of stevia to support bacterial metabolism highlights previously unrecognised interactions between dietary sweeteners and clinical bacterial isolates, with potential implications for gut health and the microbiome.