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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 of the United States of America
Vol. 101, No. 10 (Mar. 9, 2004), pp. 3587-3590
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3371523
Page Count: 4
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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.
Proceedings of the National Academy of Sciences of the United States of America © 2004 National Academy of Sciences