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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Inactivation of a Pseudomonas aeruginosa quorum-sensing signal by human airway epithelia
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Inactivation of a Pseudomonas aeruginosa quorum-sensing signal by human airway epithelia

机译：人类气道上皮细胞灭活铜绿假单胞菌群体感应信号

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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. [References: 37]
机译：哺乳动物气道通过使用多种防御机制（包括抗菌肽，粘膜纤毛清除作用和吞噬细胞）来保护自己免受细菌感染。我们询问了气道是否也可能针对关键的细菌细胞间通讯系统，即群体感应。机会病原性铜绿假单胞菌使用两个群体感应分子N-（3-氧十二烷酰基）-L-高丝氨酸内酯（30C12-HSL）和N-丁酸-L-高丝氨酸内酯（C4-HSL）来控制细胞外毒力的产生因素和生物膜形成。我们发现分化的人气道上皮细胞可以灭活30C12-HSL。对于具有某些酰基侧链的酰基-HSL，灭活是选择性的，而C4-HSL未被灭活。另外，灭活能力在不同细胞类型中差异很大。 30C12-HSL通过细胞相关活性而非分泌因子而失活。这些数据表明，人类气道上皮使群体感应信号分子失活的能力可能在抵抗细菌感染的先天防御中起作用。 [参考：37]

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