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Aminoglycosides enhance the adherence of Staphylococcus aureus to HeLa cells

Y Miyake1, A Kohada, I Fujii

  • 1Department of Microbiology, Hiroshima University School of Dentistry, Japan.

Insights

Sub-lethal aminoglycoside antibiotics increase Staphylococcus aureus adherence to human cells and extracellular matrix proteins. This effect is linked to changes in bacterial cell surface properties, not lipoteichoic acid or zeta-potential.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pharmacology

Background:

  • Staphylococcus aureus is a common human pathogen.
  • Antibiotic resistance is a growing concern.
  • Understanding bacterial adherence is crucial for infection control.

Purpose of the Study:

  • To investigate the effect of sub-lethal antibiotic concentrations on Staphylococcus aureus adherence.
  • To determine if different antibiotic classes have varying effects on adherence.
  • To explore the mechanisms underlying antibiotic-induced changes in bacterial adherence.

Main Methods:

  • Exposing Staphylococcus aureus FDA 209P to sub-lethal concentrations of various antibiotics (aminoglycosides, beta-lactams, pyridone carboxylic acid derivatives, chloramphenicol).
  • Assessing bacterial adherence to HeLa cells and immobilized fibronectin and laminin.
  • Analyzing changes in bacterial cell surface hydrophilicity and zeta-potential.
  • Investigating the role of lipoteichoic acid in bacterial adherence.

Main Results:

  • Aminoglycosides, but not other tested antibiotics, significantly enhanced Staphylococcus aureus adherence to HeLa cells.
  • Aminoglycoside treatment also increased adherence to fibronectin and laminin.
  • Bacterial cell surface hydrophilicity increased after aminoglycoside treatment.
  • Lipoteichoic acid did not inhibit adherence, and no correlation was found between adherence and zeta-potential.

Conclusions:

  • Sub-lethal aminoglycosides promote Staphylococcus aureus adherence by altering cell surface properties.
  • This enhanced adherence may contribute to increased virulence or infection persistence.
  • Further research is needed to elucidate the precise molecular mechanisms involved.

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