ArticleMolecular microbiology2011
The Pseudomonas aeruginosa flagellum confers resistance to pulmonary surfactant protein-A by impacting the production of exoproteases through quorum-sensing.
Article in Molecular microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- A nomogram for predicting neonatal acute respiratory distress syndrome in patients with neonatal pneumonia after 34 weeks of gestation.Frontiers in pediatrics · 2024Article
- Association Between Albumin Levels and Neonatal Acute Respiratory Distress Syndrome in Newborn Pneumoniae.Journal of inflammation research · 2024Article
- Mammals' humoral immune proteins and peptides targeting the bacterial envelope: from natural protection to therapeutic applications against multidrug-resistant Gram-negatives.Biological reviews of the Cambridge Philosophical Society · 2022Review
- An Organ System-Based Synopsis ofVirulence · 2021Review
- Random Peptide Mixtures as Safe and Effective Antimicrobials againstACS infectious diseases · 2021Article
- Estimation of pathogenic potential of an environmental Pseudomonas aeruginosa isolate using comparative genomics.Scientific reports · 2021Article
- Surfactant phospholipids act as molecular switches for premature induction of quorum sensing-dependent virulence inVirulence · 2020Article
- Interactions of particulate matter and pulmonary surfactant: Implications for human health.Advances in colloid and interface science · 2020Review
- Collectins: Innate Immune Pattern Recognition Molecules.Advances in experimental medicine and biology · 2020Review
- Out-Smarting the Host: Bacteria Maneuvering the Immune Response to Favor Their Survival.Frontiers in immunology · 2020Review
- The Role of Collectins and Galectins in Lung Innate Immune Defense.Frontiers in immunology · 2018Review
- Review
- A Putative ABC Transporter Permease Is Necessary for Resistance to Acidified Nitrite and EDTA in Pseudomonas aeruginosa under Aerobic and Anaerobic Planktonic and Biofilm Conditions.Frontiers in microbiology · 2016Article
- Flagellin FliC Phosphorylation Affects Type 2 Protease Secretion and Biofilm Dispersal in Pseudomonas aeruginosa PAO1.PloS one · 2016Article
- The Role of Surfactant in Lung Disease and Host Defense against Pulmonary Infections.Annals of the American Thoracic Society · 2015Review
- Type IV pilus glycosylation mediates resistance of Pseudomonas aeruginosa to opsonic activities of the pulmonary surfactant protein A.Infection and immunity · 2015Article
- Type IV pilus of Pseudomonas aeruginosa confers resistance to antimicrobial activities of the pulmonary surfactant protein-A.Journal of innate immunity · 2014Article
- Deep sequencing analyses expands the Pseudomonas aeruginosa AmpR regulon to include small RNA-mediated regulation of iron acquisition, heat shock and oxidative stress response.Nucleic acids research · 2014Article
- Themes and Variations: Regulation of RpoN-Dependent Flagellar Genes across Diverse Bacterial Species.Scientifica · 2014Review
- An Insight into the Diverse Roles of Surfactant Proteins, SP-A and SP-D in Innate and Adaptive Immunity.Frontiers in immunology · 2012Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Surfactant protein-A (SP-A) is an important antimicrobial protein that opsonizes and permeabilizes membranes of microbial pathogens in mammalian lungs. Previously, we have shown that Pseudomonas aeruginosa flagellum-deficient mutants are preferentially cleared in the lungs of wild-type mice by SP-A-mediated membrane permeabilization, and not by opsonization. In this study, we report a flagellum-mediated mechanism of P. aeruginosa resistance to SP-A. We discovered that flagellum-deficient (ΔfliC) bacteria are unable to produce adequate amounts of exoproteases to degrade SP-A in vitro and in vivo, leading to its preferential clearance in the lungs of SP-A(+/+) mice. In addition, ΔfliC bacteria failed to degrade another important lung antimicrobial protein lysozyme. Detailed analyses showed that ΔfliC bacteria are unable to upregulate the transcription of lasI and rhlI genes, impairing the production of homoserine lactones necessary for quorum-sensing, an important virulence process that regulates the production of multiple exoproteases. Thus, reduced ability of ΔfliC bacteria to quorum-sense attenuates production of exoproteases and limits degradation of SP-A, thereby conferring susceptibility to this major pulmonary host defence protein.
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Registered trials
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.