Extracellular DNA release, quorum sensing, and PrrF1/F2 small RNAs are key players in Pseudomonas aeruginosa tobramycin-enhanced biofilm formation.,npj Biofilms and Microbiomes

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Extracellular DNA release, quorum sensing, and PrrF1/F2 small RNAs are key players in Pseudomonas aeruginosa tobramycin-enhanced biofilm formation.
npj Biofilms and Microbiomes ( IF 7.8 ) Pub Date : 2019-05-23 , DOI: 10.1038/s41522-019-0088-3
Ali Tahrioui ₁ , Rachel Duchesne ₁ , Emeline Bouffartigues ₁ , Sophie Rodrigues ₁ , Olivier Maillot ₁ , Damien Tortuel ₁ , Julie Hardouin ₂ , Laure Taupin ₃ , Marie-Christine Groleau ₄ , Alain Dufour ₃ , Eric Déziel ₄ , Gerald Brenner-Weiss ₅ , Marc Feuilloley ₁ , Nicole Orange ₁ , Olivier Lesouhaitier ₁ , Pierre Cornelis ₁ , Sylvie Chevalier ₁

Affiliation

Biofilms are structured microbial communities that are the leading cause of numerous chronic infections which are difficult to eradicate. Within the lungs of individuals with cystic fibrosis (CF), Pseudomonas aeruginosa causes persistent biofilm infection that is commonly treated with aminoglycoside antibiotics such as tobramycin. However, sublethal concentrations of this aminoglycoside were previously shown to increase biofilm formation by P. aeruginosa, but the underlying adaptive mechanisms still remain elusive. Herein, we combined confocal laser scanning microscope analyses, proteomics profiling, gene expression assays and phenotypic studies to unravel P. aeruginosa potential adaptive mechanisms in response to tobramycin exposure during biofilm growth. Under this condition, we show that the modified biofilm architecture is related at least in part to increased extracellular DNA (eDNA) release, most likely as a result of biofilm cell death. Furthermore, the activity of quorum sensing (QS) systems was increased, leading to higher production of QS signaling molecules. We also demonstrate upon tobramycin exposure an increase in expression of the PrrF small regulatory RNAs, as well as expression of iron uptake systems. Remarkably, biofilm biovolumes and eDNA relative abundances in pqs and prrF mutant strains decrease in the presence of tobramycin. Overall, our findings offer experimental evidences for a potential adaptive mechanism linking PrrF sRNAs, QS signaling, biofilm cell death, eDNA release, and tobramycin-enhanced biofilm formation in P. aeruginosa. These specific adaptive mechanisms should be considered to improve treatment strategies against P. aeruginosa biofilm establishment in CF patients' lungs.

中文翻译：

细胞外DNA释放，群体感应和PrrF1 / F2小RNA是铜绿假单胞菌妥布霉素增强生物膜形成的关键因素。

生物膜是结构化的微生物群落，是许多难以根除的慢性感染的主要原因。在患有囊性纤维化（CF）的个体的肺部，铜绿假单胞菌会引起持续的生物膜感染，通常用氨基糖苷类抗生素（如妥布霉素）治疗。然而，先前已证明亚致死浓度的这种氨基糖苷会增加铜绿假单胞菌的生物膜形成，但是潜在的适应性机制仍然难以捉摸。在这里，我们结合了共聚焦激光扫描显微镜分析，蛋白质组学分析，基因表达分析和表型研究，以揭示铜绿假单胞菌潜在的适应机制，以应对生物膜生长过程中妥布霉素的暴露。在这种情况下我们表明，修改后的生物膜结构至少部分与增加的细胞外DNA（eDNA）释放有关，这很可能是生物膜细胞死亡的结果。此外，群体感应（QS）系统的活动增加了，从而导致更高的QS信号分子产生。我们还证明了妥布霉素暴露后PrrF小调控RNA表达的增加以及铁摄取系统的表达。值得注意的是，在存在妥布霉素的情况下，pqs和prrF突变菌株中的生物膜生物量和eDNA相对丰度降低。总体而言，我们的发现为铜绿假单胞菌中连接PrrF sRNA，QS信号传导，生物膜细胞死亡，eDNA释放和妥布霉素增强生物膜形成的潜在适应性机制提供了实验证据。

更新日期：2019-05-23

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