Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells.
Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells.
复制标题
囊性纤维化气道中铜绿假单胞菌细胞包膜的修饰改变了与免疫细胞的相互作用。
DOI：
10.1038/s41598-017-05253-9
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发表时间：
2017
影响因子：
4.6
通讯作者：
Torrelles,JordiB
中科院分区：
文献类型：
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作者：
Hill,PrestonJ;Scordo,JuliaM;Arcos,Jesús;Kirkby,StephenE;Wewers,MarkD;Wozniak,DanielJ;Torrelles,JordiB
铜绿假单胞菌是一种普遍存在的环境生物和机会性病原体，可引起囊性纤维化（CF）患者以及其他免疫功能低下个体的气道慢性肺部感染。在感染期间,P。铜绿杆菌进入末端细支气管和肺泡，并与肺泡内衬液（ALF）接触，其中含有稳态和抗菌水解活性，称为水解酶。这些水解酶包括一系列脂肪酶、糖苷酶和蛋白酶，因此，它们具有修饰入侵微生物表面的脂质、碳水化合物和蛋白质的潜力。我们发现健康人ALF与CF患者的水解酶水平不同。CF-ALF影响p。通过降低其中一种主要多糖Psl的含量来降低铜绿糖囊细胞壁。这种CF-ALF诱导的Psl减少不会改变细菌对表面的初始附着，但会减少生物膜的形成。重要的是，暴露于p。绿脓杆菌CF-ALF驱动中性粒细胞活化并触发其氧化反应；因此，将人类CF-ALF定义为控制p的一种新的先天防御机制。铜绿杆菌感染，但同时可能增加CF患者肺部的慢性炎症状态。
Pseudomonas aeruginosais a ubiquitous environmental organism and an opportunistic pathogen that causes chronic lung infections in the airways of cystic fibrosis (CF) patients as well as other immune-compromised individuals. During infection,P.aeruginosaenters the terminal bronchioles and alveoli and comes into contact with alveolar lining fluid (ALF), which contains homeostatic and antimicrobial hydrolytic activities, termed hydrolases. These hydrolases comprise an array of lipases, glycosidases, and proteases and thus, they have the potential to modify lipids, carbohydrates and proteins on the surface of invading microbes. Here we show that hydrolase levels between human ALF from healthy and CF patients differ. CF-ALF influences theP.aeruginosacell wall by reducing the content of one of its major polysaccharides, Psl. This CF-ALF induced Psl reduction does not alter initial bacterial attachment to surfaces but reduces biofilm formation. Importantly, exposure ofP.aeruginosato CF-ALF drives the activation of neutrophils and triggers their oxidative response; thus, defining human CF-ALF as a new innate defense mechanism to controlP.aeruginosainfection, but at the same time potentially adding to the chronic inflammatory state of the lung in CF patients.