Journal article
Paraoxonase-2 deficiency enhances Pseudomonas aeruginosa quorum sensing in murine tracheal epithelia
American journal of physiology. Lung cellular and molecular physiology, Vol.292(4), pp.L852-860
04/2007
DOI: 10.1152/ajplung.00370.2006
PMID: 17122353
Abstract
Pseudomonas aeruginosa is an important cause of nosocomial infections and is frequently present in the airways of cystic fibrosis patients. Quorum sensing mediates P. aeruginosa's virulence and biofilm formation through density-dependent interbacterial signaling with autoinducers. N-3-oxododecanoyl homoserine lactone (3OC12-HSL) is the major autoinducer in P. aeruginosa. We have previously shown that human airway epithelia and paraoxonases (PONs) degrade 3OC12-HSL. This study investigated the role of PON1, PON2, and PON3 in airway epithelial cell inactivation of 3OC12-HSL. All three PONs were present in murine tracheal epithelial cells, with PON2 and PON3 expressed at the highest levels. Lysates of tracheal epithelial cells from PON2, but not PON1 or PON3, knockout mice had impaired 3OC12-HSL inactivation compared with wild-type mice. In contrast, PON1-, PON2-, or PON3-targeted deletions did not affect 3OC12-HSL degradation by intact epithelia. Overexpression of PON2 enhanced 3OC12-HSL degradation by human airway epithelial cell lysates but not by intact epithelia. Finally, using a quorum-sensing reporter strain of P. aeruginosa, we found that quorum sensing was enhanced in PON2-deficient airway epithelia. In summary, these results show that loss of PON2 impairs 3OC12-HSL degradation by airway epithelial cells and suggests that diffusion of 3OC12-HSL into the airway cells can be the rate-limiting step for degradation of the molecule.
Details
- Title: Subtitle
- Paraoxonase-2 deficiency enhances Pseudomonas aeruginosa quorum sensing in murine tracheal epithelia
- Creators
- David A Stoltz - Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, 440 EMRB, Iowa City, IA 52242, USAEgon A OzerCarey J NgJanet M YuSrinivasa T ReddyAldons J LusisNoam BourquardMatthew R ParsekJoseph ZabnerDiana M Shih
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Lung cellular and molecular physiology, Vol.292(4), pp.L852-860
- Publisher
- United States
- DOI
- 10.1152/ajplung.00370.2006
- PMID
- 17122353
- ISSN
- 1040-0605
- eISSN
- 1522-1504
- Grant note
- P01 HL-30568 / NHLBI NIH HHS HL-61234-08 / NHLBI NIH HHS T32 GM007337 / NIGMS NIH HHS R01 HL-71776 / NHLBI NIH HHS
- Language
- English
- Date published
- 04/2007
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Molecular Physiology and Biophysics; Pulmonary, Critical Care, and Occupational Medicine; Internal Medicine
- Record Identifier
- 9984025363802771
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