Pseudomonas aeruginosa: Host defence in lung diseases

Bryan J Williams, Joanne Dehnbostel, Timothy S. Blackwell

Research output: Contribution to journalReview article

113 Scopus citations


Lung infections caused by the opportunistic pathogen Pseudomonas aeruginosa can present as a spectrum of clinical entities from a rapidly fatal pneumonia in a neutropenic patient to a multi-decade bronchitis in patients with cystic fibrosis. P. aeruginosa is ubiquitous in our environment, and one of the most versatile pathogens studied, capable of infecting a number of diverse life forms and surviving harsh environmental factors. It is also able to quickly adapt to new environments, including the lung, where it orchestrates virulence factors to acquire necessary nutrients, and if necessary, turn them off to prevent immune recognition. Despite these capabilities, P. aeruginosa rarely infects healthy human lungs. This is secondary to a highly evolved host defence mechanism that efficiently removes inhaled or aspirated pseudomonads. Many arms of the respiratory host defence have been elucidated using P. aeruginosa as a model pathogen. Human infections with P. aeruginosa have demonstrated the importance of the mechanical barrier functions including mucus clearance, and the innate immune system, including the critical role of the neutrophilic response. As more models of persistent or biofilm P. aeruginosa infections are developed, the role of the adaptive immune response will likely become more evident. Understanding the pathogenesis of P. aeruginosa, and the respiratory host defence response to it has, and will continue to, lead to novel therapeutic strategies to help patients.

Original languageEnglish (US)
Pages (from-to)1037-1056
Number of pages20
Issue number7
StatePublished - Oct 2010


  • Pseudomonas aeruginosa
  • biofilm
  • innate immunity
  • mucosal immunity
  • respiratory infection

Fingerprint Dive into the research topics of 'Pseudomonas aeruginosa: Host defence in lung diseases'. Together they form a unique fingerprint.

Cite this