Inactivation of a Pseudomonas aeruginosa quorum-sensing signal by human airway epithelia
Inactivation of a Pseudomonas aeruginosa quorum-sensing signal by human airway epithelia
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DOI：
10.1073/pnas.0308750101
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发表时间：
2004-03-09
影响因子：
11.1
通讯作者：
Greenberg, EP
中科院分区：
文献类型：
--
作者：
Chun, CK;Ozer, EA;Greenberg, EP
哺乳动物气道通过使用多种防御机制保护自身免受细菌感染，包括抗微生物肽、粘膜纤毛清除和吞噬细胞。我们问气道是否也可能针对一个关键的细菌细胞间通讯系统，群体感应。条件致病菌铜绿假单胞菌使用两种群体感应分子，N-（3-氧代十二烷酰基）-L-高丝氨酸内酯（30 C12-HSL）和N-丁酰基-L-高丝氨酸内酯（C4-HSL），来控制细胞外毒力因子的产生和生物膜的形成。我们发现分化的人气道上皮细胞使30 C12-HSL失活。灭活对具有某些酰基侧链的酰基-HSL具有选择性，并且C4-HSL未被灭活。此外，不同细胞类型的失活能力差异很大。30 C12-HSL被细胞相关活性而非分泌因子灭活。这些数据表明，人类气道上皮细胞对细菌感应信号分子的能力可能在抵抗细菌感染的先天防御中发挥作用。
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.