<p>Artificial sweeteners are widely used sugar substitutes, yet their effects on bacterial physiology and antimicrobial resistance dissemination remain poorly understood. This study evaluated the impact of the sucralose-based artificial sweetener Zerocal on bacterial growth, biofilm formation, and plasmid-mediated gene transfer in gut-associated opportunistic bacteria including extended-spectrum β-lactamase producing <i>Escherichia coli</i>, <i>Escherichia coli</i>, <i>Klebsiella pneumoniae</i>, and <i>Enterococcus faecalis</i>. Bacterial growth was monitored spectrophotometrically, biofilm formation was quantified using a crystal violet assay, and conjugative plasmid transfer was assessed using donor–recipient co-culture experiments. Exposure to Zerocal at 0.5 mM and 1 mM did not significantly alter planktonic growth of any tested strain during 24&#xa0;h incubation. In contrast, Zerocal markedly enhanced biofilm formation in a strain-dependent manner. <i>K. pneumoniae</i> exhibited the greatest increase, with biofilm biomass rising by approximately 260% at 0.5 mM and ~ 200% at 1 mM relative to controls. ESBL <i>E. coli</i> and <i>E. faecalis</i> showed increases of approximately 222% and ~ 150%, respectively, whereas no change was observed in <i>E. coli</i>. Zerocal also significantly enhanced conjugative plasmid transfer from <i>K. pneumoniae</i> to <i>E. coli</i>, increasing the number of transconjugants by 61.7% at 12&#xa0;h compared with untreated controls. Co-exposure with 0.1 mM zinc sulfate reduced Zerocal-associated biofilm formation and partially attenuated conjugation. Together, these results suggest that sucralose-containing sweeteners may promote bacterial traits associated with persistence and antimicrobial resistance dissemination. These findings raise the possibility that widely consumed artificial sweeteners may unintentionally influence bacterial traits associated with persistence and antimicrobial resistance dissemination within the gut environment.</p> Graphical abstract <p></p>

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A sucralose-based sweetener promotes biofilm formation and plasmid-mediated antibiotic resistance transfer in opportunistic gut bacteria

  • Ananya Biswas,
  • Md Hafizur Rahman,
  • Havovi Chichger,
  • Aparna Shil

摘要

Artificial sweeteners are widely used sugar substitutes, yet their effects on bacterial physiology and antimicrobial resistance dissemination remain poorly understood. This study evaluated the impact of the sucralose-based artificial sweetener Zerocal on bacterial growth, biofilm formation, and plasmid-mediated gene transfer in gut-associated opportunistic bacteria including extended-spectrum β-lactamase producing Escherichia coli, Escherichia coli, Klebsiella pneumoniae, and Enterococcus faecalis. Bacterial growth was monitored spectrophotometrically, biofilm formation was quantified using a crystal violet assay, and conjugative plasmid transfer was assessed using donor–recipient co-culture experiments. Exposure to Zerocal at 0.5 mM and 1 mM did not significantly alter planktonic growth of any tested strain during 24 h incubation. In contrast, Zerocal markedly enhanced biofilm formation in a strain-dependent manner. K. pneumoniae exhibited the greatest increase, with biofilm biomass rising by approximately 260% at 0.5 mM and ~ 200% at 1 mM relative to controls. ESBL E. coli and E. faecalis showed increases of approximately 222% and ~ 150%, respectively, whereas no change was observed in E. coli. Zerocal also significantly enhanced conjugative plasmid transfer from K. pneumoniae to E. coli, increasing the number of transconjugants by 61.7% at 12 h compared with untreated controls. Co-exposure with 0.1 mM zinc sulfate reduced Zerocal-associated biofilm formation and partially attenuated conjugation. Together, these results suggest that sucralose-containing sweeteners may promote bacterial traits associated with persistence and antimicrobial resistance dissemination. These findings raise the possibility that widely consumed artificial sweeteners may unintentionally influence bacterial traits associated with persistence and antimicrobial resistance dissemination within the gut environment.

Graphical abstract