pubmed-article:14970327 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:14970327 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:14970327 | lifeskim:mentions | umls-concept:C0033809 | lld:lifeskim |
pubmed-article:14970327 | lifeskim:mentions | umls-concept:C0014609 | lld:lifeskim |
pubmed-article:14970327 | lifeskim:mentions | umls-concept:C0458827 | lld:lifeskim |
pubmed-article:14970327 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:14970327 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:14970327 | pubmed:dateCreated | 2004-3-10 | lld:pubmed |
pubmed-article:14970327 | pubmed:abstractText | 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. | lld:pubmed |
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pubmed-article:14970327 | pubmed:language | eng | lld:pubmed |
pubmed-article:14970327 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14970327 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:14970327 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:14970327 | pubmed:month | Mar | lld:pubmed |
pubmed-article:14970327 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:14970327 | pubmed:author | pubmed-author:GreenbergE... | lld:pubmed |
pubmed-article:14970327 | pubmed:author | pubmed-author:WelshMichael... | lld:pubmed |
pubmed-article:14970327 | pubmed:author | pubmed-author:ZabnerJosephJ | lld:pubmed |
pubmed-article:14970327 | pubmed:author | pubmed-author:ChunCarlene... | lld:pubmed |
pubmed-article:14970327 | pubmed:author | pubmed-author:OzerEgon AEA | lld:pubmed |
pubmed-article:14970327 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:14970327 | pubmed:day | 9 | lld:pubmed |
pubmed-article:14970327 | pubmed:volume | 101 | lld:pubmed |
pubmed-article:14970327 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:14970327 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:14970327 | pubmed:pagination | 3587-90 | lld:pubmed |
pubmed-article:14970327 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:14970327 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:14970327 | pubmed:articleTitle | Inactivation of a Pseudomonas aeruginosa quorum-sensing signal by human airway epithelia. | lld:pubmed |
pubmed-article:14970327 | pubmed:affiliation | Pacific Biomedical Research Center, Kewalo Marine Laboratory, 41 Ahui Street, University of Hawaii, Honolulu, HI 96813, USA. | lld:pubmed |
pubmed-article:14970327 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:14970327 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:14970327 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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