Optimized alveolar epithelial cell model for chronic Pseudomonas aeruginosa and Staphylococcus aureus coinfections

Joana Admella1,2, Júlia Alcàcer-Almansa1,2, Esther Julián3

  • 1Bacterial Infections and Antimicrobial Therapies Group, Institute for Bioengineering of Catalonia (IBEC), The Barcelona Institute of Science and Technology, Barcelona, Spain.

Iscience
|October 27, 2025
PubMed

Insights

This study developed an improved in vitro model for studying Pseudomonas aeruginosa chronic respiratory infections. The model allows for longer observation periods, aiding research into P. aeruginosa and Staphylococcus aureus interactions and antibiotic effectiveness.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Biofilm Research

Background:

  • Pseudomonas aeruginosa is a key pathogen in chronic respiratory infections, often forming biofilms that complicate in vitro modeling and treatment.
  • The co-occurrence of P. aeruginosa and Staphylococcus aureus is common in cystic fibrosis patients.
  • Existing in vitro models struggle with P. aeruginosa's rapid toxin secretion, limiting study duration.

Purpose of the Study:

  • To develop a reliable and extended in vitro model for studying chronic Pseudomonas aeruginosa infections.
  • To investigate host-pathogen interactions involving P. aeruginosa and its relationship with Staphylococcus aureus.
  • To evaluate the efficacy of ciprofloxacin treatment against P. aeruginosa in the developed model.

Main Methods:

  • Optimized A549 cell culture conditions using bovine serum albumin (BSA) and extracellular matrix proteins.
  • Established P. aeruginosa biofilms within the enhanced in vitro model.
  • Studied host-pathogen interactions and bacterial co-colonization dynamics.
  • Assessed ciprofloxacin's impact on bacterial susceptibility and strain differences.

Main Results:

  • Enhanced A549 cell viability for up to 30 hours post-infection, extending study capabilities.
  • Successful development of P. aeruginosa biofilms and exploration of host-pathogen interactions.
  • Insights into the P. aeruginosa and Staphylococcus aureus relationship within the model.
  • Observed variations in ciprofloxacin susceptibility among different bacterial strains.

Conclusions:

  • The optimized in vitro model provides a robust platform for studying long-term P. aeruginosa infections and co-infections.
  • The model facilitates deeper understanding of host-pathogen dynamics and antibiotic responses.
  • Findings highlight the importance of considering bacterial strain variability in treatment strategies.

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