Inactivation of a Pseudomonas aeruginosa Quorum-Sensing Signal by Human Airway Epithelia

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 opportunist...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2004-03, Vol.101 (10), p.3587-3590
Main Authors: Chun, Carlene K., Ozer, Egon A., Welsh, Michael J., Zabner, Joseph, Greenberg, E. P.
Format: Article
Language:English
Subjects:
4-Butyrolactone - analogs & derivatives
4-Butyrolactone - antagonists & inhibitors
4-Butyrolactone - physiology
Animals
Bacteria
Biological Sciences
Biomedical research
Caco 2 cells
Cell Line
Cell lines
Cell Membrane - physiology
Cells, Cultured
Cellular biology
CHO Cells
COS Cells
Cricetinae
Cultured cells
Dogs
Epithelial cells
HeLa Cells
Homoserine - analogs & derivatives
Homoserine - antagonists & inhibitors
Homoserine - physiology
Humans
Immunity, Innate
Immunology
Infections
Kidneys
Lactones
Lungs
Pathogens
Pseudomonas aeruginosa
Pseudomonas aeruginosa - immunology
Pseudomonas aeruginosa - pathogenicity
Pseudomonas aeruginosa - physiology
Respiratory Mucosa - immunology
Respiratory Mucosa - microbiology
Respiratory system
Signal Transduction
Virulence - physiology
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Summary: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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0308750101