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

被引:209
作者
Chun, CK
Ozer, EA
Welsh, MJ
Zabner, J
Greenberg, EP [1 ]
机构
[1] Univ Iowa, Roy J & Lucille A Carver Coll Med, W M Keck Microbial Communities & Cell Signaling P, Dept Microbiol, Iowa City, IA 52242 USA
[2] Univ Iowa, Roy J & Lucille A Carver Coll Med, Howard Hughes Med Inst, Iowa City, IA 52242 USA
[3] Univ Iowa, Roy J & Lucille A Carver Coll Med, Mol Biol Grad Program, Iowa City, IA 52242 USA
[4] Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Internal Med, Iowa City, IA 52242 USA
[5] Univ Hawaii, Pacific Biomed Res Ctr, Kewalo Marine Lab, Honolulu, HI 96813 USA
关键词
D O I
10.1073/pnas.0308750101
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 (30C12-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 30C12-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. 30C12-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.
引用
收藏
页码:3587 / 3590
页数:4
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