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Updated: Jul 5, 2025

Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
08:32

Development and Assessment of Intracellular Infection Models for Staphylococcus aureus

Published on: January 17, 2025

468

Extracellular vesicles from Staphylococcus aureus promote the pathogenicity of Pseudomonas aeruginosa

Phawinee Subsomwong1, Wei Teng1, Takahito Ishiai1

  • 1Department of Microbiology and Immunology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.

Microbiological Research
|January 20, 2024
PubMed

Insights

Extracellular vesicles from Staphylococcus aureus enhance Pseudomonas aeruginosa pathogenicity. These vesicles promote biofilm formation and invasion while hindering macrophage uptake, impacting chronic wound infections.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Extracellular Vesicles

Background:

  • Co-infections with Staphylococcus aureus and Pseudomonas aeruginosa are prevalent in chronic wounds.
  • The role of extracellular vesicles (EVs) in mediating synergistic effects between these bacteria is poorly understood.
  • Investigating the impact of S. aureus EVs (SaEVs) on P. aeruginosa pathogenicity is crucial for understanding chronic wound polymicrobial infections.

Purpose of the Study:

  • To elucidate the effect of SaEVs on the pathogenicity of P. aeruginosa.
  • To determine the mechanisms by which SaEVs influence P. aeruginosa virulence factors.
  • To explore the potential of SaEVs as mediators in chronic wound polymicrobial infections.

Main Methods:

  • SaEVs were isolated and characterized.
  • Fusion between SaEVs and P. aeruginosa was confirmed using lipophilic dye.
  • Differential proteomic analysis was performed on P. aeruginosa treated with and without SaEVs.
  • Assays were conducted to evaluate LPS production, biofilm formation, gene expression, epithelial cell invasion, and macrophage uptake.

Main Results:

  • SaEVs did not affect P. aeruginosa growth or antibiotic susceptibility.
  • SaEVs significantly increased lipopolysaccharide (LPS) biosynthesis, LPS production, biofilm formation, and expression of polysaccharide polymerization-related genes in P. aeruginosa.
  • SaEV-pretreated P. aeruginosa exhibited enhanced epithelial cell invasion and impaired uptake by macrophages.
  • Proteomic analysis of SaEVs identified proteins involved in host colonization, immune evasion, and nutrient acquisition.

Conclusions:

  • SaEVs act as mediators that enhance P. aeruginosa pathogenicity.
  • Mechanisms include increased LPS biosynthesis, promoted biofilm formation, enhanced epithelial cell invasion, and impaired macrophage uptake.
  • These findings highlight the significant role of SaEVs in the complex interplay of polymicrobial infections in chronic wounds.
Keywords:
Anti-phagocytosisBiofilmExtracellular vesiclesLipopolysaccharide biosynthesisPseudomonas aeruginosaStaphylococcus aureus

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