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NPJ Biofilms Microbiomes. 2019 May 23;5:15. doi: 10.1038/s41522-019-0088-3. eCollection 2019.

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

Author information

1
1Laboratoire de Microbiologie Signaux et Microenvironnement, LMSM EA4312, Normandie Université, Université de Rouen Normandie, Évreux, France.
2
Laboratoire Polymères Biopolymères Surfaces, PBS, Normandie Université, Université de Rouen Normandie, UMR 6270 CNRS, Mont Saint Aignan, France.
3
3Laboratoire de Biotechnologie et Chimie Marines, LBCM EA3884, Institut Universitaire Européen de la Mer, Université de Bretagne-Sud, Lorient, France.
4
4INRS-Institut Armand-Frappier, Laval, QC Canada.
5
5Institute of Functional Interfaces, Karlsruhe Institute of Technology, Karlsruhe, Germany.

Abstract

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.

KEYWORDS:

Antimicrobials; Biofilms; Pathogens

Conflict of interest statement

Competing interestsThe authors declare no competing interests.

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