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In cystic fibrosis (CF) airways, Pseudomonas aeruginosa forms cellular aggregates called biofilms that are thought to contribute to chronic infection. To form aggregates, P. aeruginosa can use different mechanisms, each with its own pathogenic implications. However, how they form in vivo is controversial and unclear. One mechanism involves a bacterially produced extracellular matrix that holds the aggregates together. Pel and Psl exopolysaccharides are structural and protective components of this matrix. We develop an immunohistochemical method to visualize Pel and Psl in CF sputum. We demonstrate that both exopolysaccharides are expressed in the CF airways and that the morphology of aggregates is consistent with an exopolysaccharide-dependent aggregation mechanism. We reason that the cationic exopolysaccharide Pel may interact with some of the abundant anionic host polymers in sputum. We show that Pel binds extracellular DNA (eDNA) and that this interaction likely impacts current therapies by increasing antimicrobial tolerance and protecting eDNA from digestion.
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•Pel and Psl are produced by P. aeruginosa aggregates in cystic fibrosis sputum•Attributes of in vitro biofilms are seen in clinical aggregates•Aggregate morphology is consistent with polysaccharide-dependent aggregation•Pel-DNA interactions reduce susceptibility to antibiotic and mucolytic treatments
Pseudomonas aeruginosa forms biofilm aggregates in cystic fibrosis airways. Jennings et al. demonstrate that Pel and Psl exopolysaccharides are produced by P. aeruginosa in cystic fibrosis sputum and that aggregates are consistent with a polysaccharide-dependent aggregation mechanism. Exopolysaccharide interactions with extracellular DNA increase antimicrobial tolerance and protect DNA from digestion.