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Background <p><i>Acinetobacter baumannii</i> is a multidrug-resistant pathogen known for its robust biofilm formation, leading to persistent infections and treatment failure. Traditional antibiotics often struggle to penetrate these biofilms. Cinnamaldehyde, a plant-derived antimicrobial compound, holds potential as an antibiofilm agent. This study investigates its effects on biofilm formation, EPS production, cell surface properties, oxidative stress response, and gene expression in <i>A. baumannii.</i></p> Methods <p>This study evaluated the antibiofilm activity of cinnamaldehyde using <i>A. baumannii</i>. Biofilm formation was quantified via crystal violet assay, while structural alterations were visualised using light microscopy, SEM, and CLSM. EPS production and cell surface hydrophobicity were evaluated using phenol-sulfuric acid and MATH assays. Catalase activity was assessed through H₂O₂ sensitivity, and qRT-PCR analysed gene expression. Cytotoxicity was evaluated using the MTT assay on mouse fibroblast cells.</p> Results <p>Cinnamaldehyde significantly inhibited biofilm formation, with 86.67% reduction at 0.007% (v/v), without affecting planktonic growth. Microscopy revealed disrupted biofilm architecture and reduced microcolony formation. SEM showed reduced EPS and altered cell morphology. EPS quantification confirmed a 33.06% reduction. Cell surface hydrophobicity decreased from 86.76% to 21.93%, impairing bacterial adhesion. H₂O₂ sensitivity increased, indicating reduced catalase activity. Gene expression analysis showed downregulation of <i>bfmR</i>, <i>ompA</i>, <i>csuA</i>/<i>B</i>, and <i>katE</i>. Cinnamaldehyde showed minimal cytotoxicity in mouse fibroblast cells.</p> Conclusion <p>Cinnamaldehyde effectively inhibits <i>A. baumannii</i> biofilms through structural disruption, EPS reduction, altered surface hydrophobicity, oxidative stress sensitization, and gene suppression. Its non-toxic nature and broad mechanisms highlight its potential as a plant-based antibiofilm agent for controlling resistant infections.</p>

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Antibiofilm and antivirulence effects of cinnamaldehyde on Acinetobacter baumannii

  • 期刊论文

  • 发表日期：

    2026年6月24日

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  • Thahiya Naushad,
  • Sajna Salim,
  • Shiburaj Sugathan,
  • Irfan Türetgen

摘要

Background

Acinetobacter baumannii is a multidrug-resistant pathogen known for its robust biofilm formation, leading to persistent infections and treatment failure. Traditional antibiotics often struggle to penetrate these biofilms. Cinnamaldehyde, a plant-derived antimicrobial compound, holds potential as an antibiofilm agent. This study investigates its effects on biofilm formation, EPS production, cell surface properties, oxidative stress response, and gene expression in A. baumannii.

Methods

This study evaluated the antibiofilm activity of cinnamaldehyde using A. baumannii. Biofilm formation was quantified via crystal violet assay, while structural alterations were visualised using light microscopy, SEM, and CLSM. EPS production and cell surface hydrophobicity were evaluated using phenol-sulfuric acid and MATH assays. Catalase activity was assessed through H₂O₂ sensitivity, and qRT-PCR analysed gene expression. Cytotoxicity was evaluated using the MTT assay on mouse fibroblast cells.

Results

Cinnamaldehyde significantly inhibited biofilm formation, with 86.67% reduction at 0.007% (v/v), without affecting planktonic growth. Microscopy revealed disrupted biofilm architecture and reduced microcolony formation. SEM showed reduced EPS and altered cell morphology. EPS quantification confirmed a 33.06% reduction. Cell surface hydrophobicity decreased from 86.76% to 21.93%, impairing bacterial adhesion. H₂O₂ sensitivity increased, indicating reduced catalase activity. Gene expression analysis showed downregulation of bfmR, ompA, csuA/B, and katE. Cinnamaldehyde showed minimal cytotoxicity in mouse fibroblast cells.

Conclusion

Cinnamaldehyde effectively inhibits A. baumannii biofilms through structural disruption, EPS reduction, altered surface hydrophobicity, oxidative stress sensitization, and gene suppression. Its non-toxic nature and broad mechanisms highlight its potential as a plant-based antibiofilm agent for controlling resistant infections.