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<p>The development of innovative methods for quantitatively assessing drug efficacy is essential for advancing effective treatments against antibiotic-resistant bacteria. A key determinant of drug activity against resistant Gram-negative bacteria is the permeability of the bacterial cell envelope, particularly that of the outer membrane, which is the first line of defense against antimicrobials. In this study, we report a method to quantitatively evaluate outer membrane permeability to β-lactams (nitrocefin, mecillinam, cloxacillin) and to a β-lactamase inhibitor (avibactam) by monitoring their entry into outer membrane vesicles (OMVs) produced by <i>Escherichia coli</i> and <i>Pseudomonas aeruginosa</i>. We also show that drug-susceptible bacteria are effectively shielded from β-lactams by OMVs emanating from resistant bacteria that contain a periplasmic β-lactamase captured upon their formation. Altogether, our work provides a comprehensive framework for understanding how antimicrobial molecules interact with bacterial OMVs and how this process contributes to the spread of antibiotic resistance.</p>

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Quantifying outer membrane permeability to β-lactam antibiotics using outer membrane vesicles that protect antibiotic-susceptible bacteria

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月22日

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  • Alicja Razew,
  • Quentin Herail,
  • Isabel Ayala,
  • Myriam Guissouma,
  • Michel Arthur,
  • Jean-Pierre Simorre

摘要

The development of innovative methods for quantitatively assessing drug efficacy is essential for advancing effective treatments against antibiotic-resistant bacteria. A key determinant of drug activity against resistant Gram-negative bacteria is the permeability of the bacterial cell envelope, particularly that of the outer membrane, which is the first line of defense against antimicrobials. In this study, we report a method to quantitatively evaluate outer membrane permeability to β-lactams (nitrocefin, mecillinam, cloxacillin) and to a β-lactamase inhibitor (avibactam) by monitoring their entry into outer membrane vesicles (OMVs) produced by Escherichia coli and Pseudomonas aeruginosa. We also show that drug-susceptible bacteria are effectively shielded from β-lactams by OMVs emanating from resistant bacteria that contain a periplasmic β-lactamase captured upon their formation. Altogether, our work provides a comprehensive framework for understanding how antimicrobial molecules interact with bacterial OMVs and how this process contributes to the spread of antibiotic resistance.