ArticleAmerican journal of respiratory and critical care medicine2011
Hemolytic phospholipase C inhibition protects lung function during Pseudomonas aeruginosa infection.
Article in American journal of respiratory and critical care medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 78 citations in OpenAlex.
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- Exploring the antimicrobial potential of chitosan nanoparticles: synthesis, characterization and impact onNanoscale advances · 2024Article
- Sphingosine induction of theJournal of bacteriology · 2024Article
- Membrane staining and phospholipid tracking in Pseudomonas aeruginosa PAO1 using the phosphatidylcholine mimic propargyl-choline.Access microbiology · 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
- Current concepts on Pseudomonas aeruginosa interaction with human airway epithelium.PLoS pathogens · 2023Review
- Phospholipase C: underrated players in microbial infections.Frontiers in cellular and infection microbiology · 2023Review
- Prevalence of Quorum Sensing and Virulence Factor Genes AmongInfection and drug resistance · 2023Article
- Targeting theFrontiers in microbiology · 2022Article
- Virulence Factors ofFrontiers in cellular and infection microbiology · 2022Review
- Role of Host and Bacterial Lipids inFrontiers in immunology · 2022Review
- Assessing a transmission network of Mycobacterium tuberculosis in an African city using single nucleotide polymorphism threshold analysis.MicrobiologyOpen · 2021Article
- Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
rationaleThe opportunistic pathogen Pseudomonas aeruginosa causes both acute and chronic lung infections and is particularly problematic in patients with cystic fibrosis and those undergoing mechanical ventilation. Decreased lung function contributes significantly to morbidity and mortality during P. aeruginosa infection, and damage inflicted by P. aeruginosa virulence factors contributes to lung function decline.
objectivesWe sought to describe direct contribution of a bacterial phospholipase C/sphingomyelinase, PlcHR, to alteration of host lung physiology and characterize a potential therapeutic for protection of lung function.
methodsWe infected C57Bl/6 mice with P. aeruginosa wild-type or isogenic plcHR deletion strains and measured lung function using computer-controlled ventilators. For in vivo testing, miltefosine was delivered intraperitoneally 1 hour after infection. Infection and respiratory endpoints were at 24 hours after infection. MEASUREMENTS AND MAIN
resultsP. aeruginosa wild-type infection caused significant lung function impairment, whereas the effects of a ΔplcHR strain infection were much less severe. Surfactometry analysis of bronchoalveolar lavage fluid indicated that PlcHR decreased pulmonary surfactant function. Miltefosine has structural similarity to the PC and sphingomyelin substrates of PlcHR, and we found that it inhibits the cleavage of these choline-containing lipids in vitro. Miltefosine administration after P. aeruginosa infection limited the negative effects of PlcHR activity on lung function.
conclusionsWe have directly linked production of a single virulence factor in P. aeruginosa with effects on lung function, and demonstrated that the inhibitor miltefosine protects lung function from PlcHR-dependent surfactant dysfunction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.