Co-evolution with Staphylococcus aureus leads to lipopolysaccharide alterations in Pseudomonas aeruginosa

Mikael Tognon1,2, Thilo Köhler1,2, Bartosz G Gdaniec1,2

  • 1Transplant Infectious Diseases Unit, University Hospitals of Geneva, Genève, Switzerland.

The ISME Journal
|May 27, 2017
PubMed

Insights

Pseudomonas aeruginosa lipopolysaccharide (LPS) mutations provide a fitness advantage when co-colonizing with Staphylococcus aureus in cystic fibrosis airways. These LPS mutations also increase resistance to beta-lactam antibiotics.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Genomics

Background:

  • Bacterial co-colonization in cystic fibrosis (CF) airways involves complex interactions influencing infection outcomes.
  • Staphylococcus aureus dominates early CF infections, with Pseudomonas aeruginosa becoming predominant later.

Purpose of the Study:

  • To investigate adaptive evolution of P. aeruginosa in response to S. aureus.
  • To determine if P. aeruginosa adaptations are specific responses to S. aureus or general environmental responses.

Main Methods:

  • Evolving P. aeruginosa populations for 150 generations in the presence and absence of S. aureus.
  • Whole-genome sequencing of evolved P. aeruginosa populations and comparison to the ancestor strain.

Main Results:

  • Mutations in the Wsp signaling system were found in both conditions, likely due to low oxygen.
  • Mutations in lipopolysaccharide (LPS) biosynthesis occurred exclusively in co-cultures with S. aureus, conferring a fitness gain.
  • LPS mutations increased resistance to beta-lactam antibiotics and were observed in clinical CF isolates.

Conclusions:

  • P. aeruginosa LPS mutations are a direct result of S. aureus-imposed selection in vitro.
  • Wsp and LPS mutations found in evolved strains are also present in clinical CF isolates, highlighting their relevance.
  • Understanding these interactions is crucial for managing chronic CF lung infections.

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