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Rapid necrotic killing of polymorphonuclear leukocytes is caused by quorum-sensing-controlled production of rhamnolipid by Pseudomonas aeruginosa.

Author information

Affiliations

  • 1. Department of Clinical Microbiology, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark.
      Authors
    • Jensen PØ 1
    • Calum H 1
    • Christoffersen L 1
    • Moser C 1
    • Høiby N 1
    (5 authors)
  • 2. Centre for Biomedical Microbiology, BioCentrum, Technical University of Denmark.
      Authors
    • Bjarnsholt T 2
    • Phipps R 2
    • Rasmussen TB 2
    • Givskov M 2
    (4 authors)
  • 3. Centre for Biomolecular Sciences, University of Nottingham, UK.
      Authors
    • Williams P 3
    (1 author)
  • 4. Copenhagen CF Center, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark.
      Authors
    • Pressler T 4
    (1 author)

ORCIDs linked to this article

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Microbiology (Reading, England), 01 May 2007, 153(Pt 5):1329-1338
https://doi.org/10.1099/mic.0.2006/003863-0 PMID: 17464047 

Abstract 

Quorum sensing (QS) denotes a density-dependent mode of inter-bacterial communication based on signal transmitter molecules. Active QS is present during chronic infections with the opportunistic pathogen Pseudomonas aeruginosa in immunocompromised patients. The authors have previously demonstrated a QS-regulated tolerance of biofilm bacteria to the antimicrobial properties of polymorphonuclear leukocytes (PMNs). The precise QS-regulated effect on the PMNs is, however, unknown. Incubation of human PMNs with supernatants from dense P. aeruginosa cultures showed that the QS-competent P. aeruginosa induced rapid necrosis of the PMNs. This mechanism was also observed in mouse lungs infected with P. aeruginosa, and in sputum obtained from P.-aeruginosa-infected patients with cystic fibrosis. Evidence is presented that the necrotic effect was caused by rhamnolipids, production of which is QS controlled. The results demonstrate the potential of the QS system to facilitate infections with P. aeruginosa by disabling the PMNs, which are a major first line of defence of the host. Furthermore, the study emphasizes the inhibition of QS as a target for the treatment of infections with P. aeruginosa.

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Read article at publisher's site: https://doi.org/10.1099/mic.0.2006/003863-0

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