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<p>The rise of colistin-resistant <i>Acinetobacter baumannii</i> (ColR Ab) poses a major clinical challenge, underscoring the urgent need for alternative antimicrobial agents. This study evaluated the antibacterial and anti-biofilm mechanisms of 1,8-cineole against ColR Ab using in vitro, transcriptional, and in silico approaches. Minimum inhibitory concentrations (MICs) and anti-biofilm activities were determined against three ColR Ab isolates. Membrane integrity was assessed via protein and nucleic acid leakage assays. Scanning electron microscopy (SEM) revealed bacterial morphology and biofilm structure, and expression of biofilm-associated genes was analyzed by qRT-PCR. Additionally, molecular docking analysis was employed to evaluate the binding affinity of 1,8-cineole against key target proteins of <i>A. baumannii</i>. The inhibition zone in the disk diffusion method and MIC were 10.3 ± 0.8&#xa0;mm and 3.6&#xa0;mg/mL, respectively. 1,8-cineole also caused significant protein and nucleic acid leakage and, at 4× MIC, significantly disrupted the mature biofilm structure. SEM confirmed bacterial cell membrane rupture, intracellular content leakage, and ultrastructural damage following treatment. qRT-PCR validation demonstrated that 1,8-cineole significantly downregulated the expression of the <i>bfmR</i>, <i>bap</i>, <i>csuE</i>, <i>ompA</i>, and <i>pgaB</i>, while <i>abaI</i> expression was not significantly affected. Molecular docking simulations predicted favorable binding of 1,8-cineole to quorum-sensing regulators AbaR and LasR. 1,8-cineole exhibits significant bactericidal and anti-biofilm activity against ColR Ab. Its mechanism of action may involve disruption of cell membrane integrity and potential interference with bacterial key quorum-sensing regulators. This study provides a theoretical basis for developing 1,8-cineole as a potential therapeutic strategy against ColR Ab infections.</p>

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Antibacterial and anti-biofilm mechanisms of 1,8-cineole against colistin-resistant Acinetobacter baumannii: an integrated in vitro, gene expression, and in silico study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月30日

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  • Milad Kashi,
  • Aboalhasan Basil Sami Alshemri,
  • Zahra Alimardan,
  • Mohammad Arjomandzadegan,
  • Yasaman Hariri,
  • Zahra Chegini,
  • Aref Shariati

摘要

The rise of colistin-resistant Acinetobacter baumannii (ColR Ab) poses a major clinical challenge, underscoring the urgent need for alternative antimicrobial agents. This study evaluated the antibacterial and anti-biofilm mechanisms of 1,8-cineole against ColR Ab using in vitro, transcriptional, and in silico approaches. Minimum inhibitory concentrations (MICs) and anti-biofilm activities were determined against three ColR Ab isolates. Membrane integrity was assessed via protein and nucleic acid leakage assays. Scanning electron microscopy (SEM) revealed bacterial morphology and biofilm structure, and expression of biofilm-associated genes was analyzed by qRT-PCR. Additionally, molecular docking analysis was employed to evaluate the binding affinity of 1,8-cineole against key target proteins of A. baumannii. The inhibition zone in the disk diffusion method and MIC were 10.3 ± 0.8 mm and 3.6 mg/mL, respectively. 1,8-cineole also caused significant protein and nucleic acid leakage and, at 4× MIC, significantly disrupted the mature biofilm structure. SEM confirmed bacterial cell membrane rupture, intracellular content leakage, and ultrastructural damage following treatment. qRT-PCR validation demonstrated that 1,8-cineole significantly downregulated the expression of the bfmR, bap, csuE, ompA, and pgaB, while abaI expression was not significantly affected. Molecular docking simulations predicted favorable binding of 1,8-cineole to quorum-sensing regulators AbaR and LasR. 1,8-cineole exhibits significant bactericidal and anti-biofilm activity against ColR Ab. Its mechanism of action may involve disruption of cell membrane integrity and potential interference with bacterial key quorum-sensing regulators. This study provides a theoretical basis for developing 1,8-cineole as a potential therapeutic strategy against ColR Ab infections.