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<p>Active efflux is one of the most widespread antibiotic resistance mechanisms used by bacteria to survive in the presence of bacteriostatic and bactericidal compounds. In this study, the antibacterial activity of citronellol and its potential to inhibit the NorA efflux pump in <i>Staphylococcus aureus</i> strains 1199 and 1199B were evaluated, as well as the inhibitory effect through fluorescence methods and membrane permeability. Additionally, the interactions of this compound with NorA were analyzed using molecular docking, and its pharmacokinetic properties were assessed through ADMET (Absorption, Distribution, Metabolism, Excretion, and Toxicity) modeling. The results revealed that citronellol did not exhibit direct antibacterial activity; however, when combined with norfloxacin, it enhanced its effect on the tested strains. Furthermore, citronellol reduced the minimum inhibitory concentration (MIC) of ethidium bromide (EtBr), suggesting a potential inhibition of the NorA efflux pump. These effects were corroborated by an increase in the bacterial membrane permeability of the <i>S. aureus</i> strains treated with citronellol and by the enhanced fluorescence emission of EtBr, indicating a possible effect of citronellol on the inhibition of the NorA efflux pump in <i>S. aureus</i>. Molecular docking data showed that citronellol binds to the NorA efflux pump receptor in a manner analogous to the control chlorpromazine. Pharmacokinetic data revealed that citronellol has moderate lipophilicity, enabling a balance between high cellular permeability and low hepatic clearance. Therefore, citronellol shows promising potential as an inhibitor of the resistance mechanism present in <i>S. aureus</i>.</p>

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Evaluation of the antibacterial and inhibitory activity of the NorA efflux pump in Staphylococcus aureus by citronellol

  • 期刊论文

  • 发表日期：

    2025年6月24日

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  • Alisson Justino Alves da Silva,
  • Zildene de Sousa Silveira,
  • Nair Silva Macêdo,
  • Cristina Rodrigues dos Santos Barbosa,
  • Ângella Eduarda da Silva Sousa,
  • Thaís Ferreira da Silva,
  • Josivânia Teixeira de Sousa,
  • Cícera Datiane de Morais Oliveira-Tintino,
  • Saulo Relison Tintino,
  • Emmanuel Silva Marinho,
  • Matheus Nunes da Rocha,
  • Damião Sampaio de Sousa,
  • Marcia Machado Marinho,
  • Hélcio Silva dos Santos,
  • Henrique Douglas Melo Coutinho,
  • Francisco Assis Bezerra da Cunha

摘要

Active efflux is one of the most widespread antibiotic resistance mechanisms used by bacteria to survive in the presence of bacteriostatic and bactericidal compounds. In this study, the antibacterial activity of citronellol and its potential to inhibit the NorA efflux pump in Staphylococcus aureus strains 1199 and 1199B were evaluated, as well as the inhibitory effect through fluorescence methods and membrane permeability. Additionally, the interactions of this compound with NorA were analyzed using molecular docking, and its pharmacokinetic properties were assessed through ADMET (Absorption, Distribution, Metabolism, Excretion, and Toxicity) modeling. The results revealed that citronellol did not exhibit direct antibacterial activity; however, when combined with norfloxacin, it enhanced its effect on the tested strains. Furthermore, citronellol reduced the minimum inhibitory concentration (MIC) of ethidium bromide (EtBr), suggesting a potential inhibition of the NorA efflux pump. These effects were corroborated by an increase in the bacterial membrane permeability of the S. aureus strains treated with citronellol and by the enhanced fluorescence emission of EtBr, indicating a possible effect of citronellol on the inhibition of the NorA efflux pump in S. aureus. Molecular docking data showed that citronellol binds to the NorA efflux pump receptor in a manner analogous to the control chlorpromazine. Pharmacokinetic data revealed that citronellol has moderate lipophilicity, enabling a balance between high cellular permeability and low hepatic clearance. Therefore, citronellol shows promising potential as an inhibitor of the resistance mechanism present in S. aureus.