Sweetener specific modulation of physiological responses in uropathogenic E. 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.
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.