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Updated: Jun 10, 2026

Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
Published on: March 17, 2014
Quorum sensing-dependent virulence during Pseudomonas aeruginosa colonisation and pneumonia in mechanically
Thilo Köhler1, Raphael Guanella, Jean Carlet
1Service of Infectious Diseases, University Hospital Geneva, 4 Rue Gabrielle-Perret-Gentil, Geneva 14, Switzerland.
Background:
Pseudomonas aeruginosa frequently colonises intubated patients and causes life-threatening ventilator-associated pneumonia (VAP). The role of quorum sensing (QS), regulating virulence in this pathogen, during colonisation and development of VAP is unknown.
Methods:
P aeruginosa isolates and tracheal aspirates were prospectively collected from intubated patients. Genotypes and QS-independent virulence traits (exoU, exoS, PAPI-1 and PAPI-2) harboured by colonising isolates were identified in vitro with the CLONDIAG array. The production of elastase and rhamnolipids was measured to assess QS-dependent virulence. To monitor QS activity 'in patient', total RNA was extracted directly from tracheal aspirates and expression of QS genes was measured.
Results:
320 P aeruginosa isolates and tracheal aspirates were obtained from 29 patients of whom 6 developed VAP (20%). Seven patients (24%) were initially colonised by QS-proficient isolates; 57% of them developed VAP as compared with 9% of patients colonised by QS-deficient isolates (p=0.018). Of all tested virulence traits from the initial colonising isolates, only rhamnolipids were associated with development of VAP (p=0.003). VAP occurred more frequently in patients colonised during the entire observation period by isolates producing high levels of rhamnolipids (p=0.001). 'In patient' monitoring of QS genes showed non-induced expression profiles in patients without VAP. In contrast, exponential induction of QS circuit and target gene expression was observed for two patients with VAP, and an 'in patient' QS gene expression profile and hierarchy similar to those in vitro was measured for one patient with VAP.
Conclusions:
Production of the QS-dependent virulence factor rhamnolipids by colonising P aeruginosa isolates is associated with development of VAP.
Insights
Quorum sensing (QS) in Pseudomonas aeruginosa, particularly rhamnolipid production, is linked to ventilator-associated pneumonia (VAP) development in intubated patients. QS-proficient isolates increased VAP risk, highlighting rhamnolipids as a key virulence factor.
Area of Science:
- Microbiology
- Infectious Diseases
- Critical Care Medicine
Background:
- Pseudomonas aeruginosa is a common colonizer in intubated patients, leading to severe ventilator-associated pneumonia (VAP).
- The role of quorum sensing (QS) in P. aeruginosa virulence during VAP development remains unclear.
Purpose of the Study:
- To investigate the association between quorum sensing (QS) and the development of ventilator-associated pneumonia (VAP) in intubated patients.
- To determine the role of QS-dependent virulence factors, specifically rhamnolipids, in P. aeruginosa colonization and VAP onset.
Main Methods:
- Prospective collection of P. aeruginosa isolates and tracheal aspirates from intubated patients.
- In vitro analysis of P. aeruginosa genotypes and QS-independent virulence factors (exoU, exoS, PAPI-1, PAPI-2).
- Measurement of elastase and rhamnolipid production to assess QS-dependent virulence; in-patient QS gene expression analysis via RNA extraction from tracheal aspirates.
Main Results:
- Patients colonized by QS-proficient P. aeruginosa isolates had a significantly higher risk of developing VAP (57% vs. 9%).
- Rhamnolipid production by initial colonizing isolates was strongly associated with VAP development (p=0.003).
- In-patient monitoring revealed induced QS gene expression in patients who developed VAP, mirroring in vitro findings.
Conclusions:
- Rhamnolipid production by colonizing P. aeruginosa is a significant virulence factor associated with VAP development.
- Quorum sensing activity, particularly rhamnolipid synthesis, plays a critical role in the pathogenesis of VAP.
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