ArticlePloS one2014
Blocking phosphatidylcholine utilization in Pseudomonas aeruginosa, via mutagenesis of fatty acid, glycerol and choline degradation pathways, confirms the importance of this nutrient source in vivo.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
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- An integrated computational-experimental approach identifies Malate Synthase G as therapeutic target to disrupt carbon metabolism in chronic Pseudomonas aeruginosa infection.Functional & integrative genomics · 2026Article
- Role of PsrA in physiology and virulence regulation inJournal of bacteriology · 2026Review
- Molecular Mechanisms Underlying the Pathogenicity ofMedicina (Kaunas, Lithuania) · 2026Review
- Activation of theInfection and immunity · 2025Article
- The fatty acid synthesis geneMicrobiology spectrum · 2025Article
- A glyoxal-specific aldehyde signaling axis in Pseudomonas aeruginosa that influences quorum sensing and infection.Nature communications · 2025Article
- D-Amino acids affect Pseudomonas aeruginosa biofilm and quorum sensing molecules in lung infection models developed under a cystic fibrosis environment.Scientific reports · 2025Article
- Pseudomonas aeruginosa acyl-CoA dehydrogenases and structure-guided inversion of their substrate specificity.Nature communications · 2025Article
- Biocide-resistant Pseudomonas oleovorans isolated from water-based coatings used in construction.Journal of industrial microbiology & biotechnology · 2024Article
- Bacterial acquisition of host fatty acids has far-reaching implications on virulence.Microbiology and molecular biology reviews : MMBR · 2024Review
- The Epistemology of Bacterial Virulence Factor Characterization.Microorganisms · 2024Review
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- How Does Airway Surface Liquid Composition Vary in Different Pulmonary Diseases, and How Can We Use This Knowledge to Model Microbial Infections?Microorganisms · 2024Review
- Metabolomics responses and tolerance of Pseudomonas aeruginosa under acoustic vibration stress.PloS one · 2024Article
- Regulatory and structural mechanisms of PvrA-mediated regulation of the PQS quorum-sensing system and PHA biosynthesis in Pseudomonas aeruginosa.Nucleic acids research · 2023Article
- Functional Amyloids in Pseudomonas aeruginosa Are Essential for the Proteome Modulation That Leads to Pathoadaptation in Pulmonary Niches.Microbiology spectrum · 2023Article
- Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Pseudomonas aeruginosa can grow to very high-cell-density (HCD) during infection of the cystic fibrosis (CF) lung. Phosphatidylcholine (PC), the major component of lung surfactant, has been hypothesized to support HCD growth of P. aeruginosa in vivo. The phosphorylcholine headgroup, a glycerol molecule, and two long-chain fatty acids (FAs) are released by enzymatic cleavage of PC by bacterial phospholipase C and lipases. Three different bacterial pathways, the choline, glycerol, and fatty acid degradation pathways, are then involved in the degradation of these PC components. Here, we identified five potential FA degradation (Fad) related fadBA-operons (fadBA1-5, each encoding 3-hydroxyacyl-CoA dehydrogenase and acyl-CoA thiolase). Through mutagenesis and growth analyses, we showed that three (fadBA145) of the five fadBA-operons are dominant in medium-chain and long-chain Fad. The triple fadBA145 mutant also showed reduced ability to degrade PC in vitro. We have previously shown that by partially blocking Fad, via mutagenesis of fadBA5 and fadDs, we could significantly reduce the ability of P. aeruginosa to replicate on FA and PC in vitro, as well as in the mouse lung. However, no studies have assessed the ability of mutants, defective in choline and/or glycerol degradation in conjunction with Fad, to grow on PC or in vivo. Hence, we constructed additional mutants (ΔfadBA145ΔglpD, ΔfadBA145ΔbetAB, and ΔfadBA145ΔbetABΔglpD) significantly defective in the ability to degrade FA, choline, and glycerol and, therefore, PC. The analysis of these mutants in the BALB/c mouse lung infection model showed significant inability to utilize PC in vitro, resulted in decreased replication fitness and competitiveness in vivo compared to the complement strain, although there was little to no variation in typical virulence factor production (e.g., hemolysin, lipase, and protease levels). This further supports the hypothesis that lung surfactant PC serves as an important nutrient for P. aeruginosa during CF lung infection.
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