Inactivation of a Pseudomonas aeruginosa quorum-sensing signal by human airway epithelia

Carlene K Chun; Egon A Ozer; Michael J Welsh; Joseph Zabner; E. P Greenberg

doi:10.1073/pnas.0308750101

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Inactivation of a Pseudomonas aeruginosa quorum-sensing signal by human airway epithelia

Journal article

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Inactivation of a Pseudomonas aeruginosa quorum-sensing signal by human airway epithelia

Carlene K Chun, Egon A Ozer, Michael J Welsh, Joseph Zabner and E. P Greenberg

Proceedings of the National Academy of Sciences - PNAS, Vol.101(10), pp.3587-3590

From the Cover

03/09/2004

DOI: 10.1073/pnas.0308750101

PMCID: PMC373506

PMID: 14970327

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Abstract

Mammalian airways protect themselves from bacterial infection by using multiple defense mechanisms including antimicrobial peptides, mucociliary clearance, and phagocytic cells. We asked whether airways might also target a key bacterial cell-cell communication system, quorum-sensing. The opportunistic pathogen Pseudomonas aeruginosa uses two quorum-sensing molecules, N -(3-oxododecanoyl)- l -homoserine lactone (3OC12-HSL) and N -butanoyl- l -homoserine lactone (C4-HSL), to control production of extracellular virulence factors and biofilm formation. We found that differentiated human airway epithelia inactivated 3OC12-HSL. Inactivation was selective for acyl-HSLs with certain acyl side chains, and C4-HSL was not inactivated. In addition, the capacity for inactivation varied widely in different cell types. 3OC12-HSL was inactivated by a cell-associated activity rather than a secreted factor. These data suggest that the ability of human airway epithelia to inactivate quorum-sensing signal molecules could play a role in the innate defense against bacterial infection.

Biological Sciences

Details

Title: Subtitle: Inactivation of a Pseudomonas aeruginosa quorum-sensing signal by human airway epithelia
Creators: Carlene K Chun - Pacific Biomedical Research Center, Kewalo Marine Laboratory, 41 Ahui Street, University of Hawaii, Honolulu, HI 96813; and
Egon A Ozer - Pacific Biomedical Research Center, Kewalo Marine Laboratory, 41 Ahui Street, University of Hawaii, Honolulu, HI 96813; and
Michael J Welsh - Pacific Biomedical Research Center, Kewalo Marine Laboratory, 41 Ahui Street, University of Hawaii, Honolulu, HI 96813; and
Joseph Zabner - Pacific Biomedical Research Center, Kewalo Marine Laboratory, 41 Ahui Street, University of Hawaii, Honolulu, HI 96813; and
E. P Greenberg - Pacific Biomedical Research Center, Kewalo Marine Laboratory, 41 Ahui Street, University of Hawaii, Honolulu, HI 96813; and
Resource Type: Journal article
Publication Details: Proceedings of the National Academy of Sciences - PNAS, Vol.101(10), pp.3587-3590
Series: From the Cover
DOI: 10.1073/pnas.0308750101
PMID: 14970327
PMCID: PMC373506
NLM abbreviation: Proc Natl Acad Sci U S A
ISSN: 0027-8424
eISSN: 1091-6490
Publisher: National Academy of Sciences
Language: English
Date published: 03/09/2004
Academic Unit: Neurology; Molecular Physiology and Biophysics; Pulmonary, Critical Care, and Occupational Medicine; Neurosurgery; Internal Medicine
Record Identifier: 9984020657402771

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