ArticlePloS one2009
Pseudomonas aeruginosa LPS or flagellin are sufficient to activate TLR-dependent signaling in murine alveolar macrophages and airway epithelial cells.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 167 citations in OpenAlex.
- Pseudomonas aeruginosa: associated pathogenesis, epidemiology, resistance mechanisms, host response and emerging treatment strategies.Archives of microbiology · 2026Review
- Ivermectin modulates macrophage activity and enhances bacterial clearance in Pseudomonas aeruginosa acute pneumonia.Molecular and cellular biochemistry · 2026Article
- Macrophage-induced reduction of bacteriophage density limits the efficacy of in vivo pulmonary phage therapy.Nature communications · 2025Article
- Macrophage-induced reduction of bacteriophage density limits the efficacy ofbioRxiv : the preprint server for biology · 2025Article
- Absence of c-Maf and IL-10 enables type I IFN enhancement of innate responses to LPS in alveolar macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Perturbation of EPHA2 and EFNA1iScience · 2025Article
- Article
- A comprehensive review of the pathogenic mechanisms ofFrontiers in microbiology · 2025Review
- TLR2 or TLR4 Stimulation Induces Transmembrane TNF-Driven Priming in Macrophages Which Results in Improved Clearance of a Subsequent Staphylococcus aureus Infection.Journal of innate immunity · 2025Article
- Genetically engineered phages and engineered phage-derived enzymes to destroy biofilms of antibiotics resistance bacteria.Heliyon · 2024Review
- Absence of c-Maf and IL-10 enables Type I IFN enhancement of innate responses to low-dose LPS in alveolar macrophages.bioRxiv : the preprint server for biology · 2024Article
- Antimicrobial peptide glatiramer acetate targets Pseudomonas aeruginosa lipopolysaccharides to breach membranes without altering lipopolysaccharide modification.npj antimicrobials and resistance · 2024Article
- Review
- Cold dispase digestion of murine lungs improves recovery and culture of airway epithelial cells.PloS one · 2024Article
- Battle royale: Immune response on biofilms - host-pathogen interactions.Current research in immunology · 2023Review
- Article
- P. aeruginosa type III and type VI secretion systems modulate early response gene expression in type II pneumocytes in vitro.BMC genomics · 2022Article
- IL-6-elafin genetically modified macrophages as a lung immunotherapeutic strategy against Pseudomonas aeruginosa infections.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Isthmin 1 is Expressed by Progenitor-Like Cells in the Lung: Phenotypical Analysis of Isthmin 1Journal of immunology research · 2022Article
- Tartrate resistant acid phosphatase 5 (TRAP5) mediates immune cell recruitment in a murine model of pulmonary bacterial infection.Frontiers in immunology · 2022Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe human lung is exposed to a large number of airborne pathogens as a result of the daily inhalation of 10,000 liters of air. Innate immunity is thus essential to defend the lungs against these pathogens. This defense is mediated in part through the recognition of specific microbial ligands by Toll-like receptors (TLR) of which there are at least 10 in humans. Pseudomonas aeruginosa is the main pathogen that infects the lungs of cystic fibrosis patients. Based on whole animal experiments, using TLR knockout mice, the control of this bacterium is believed to occur by the recognition of LPS and flagellin by TLRs 2,4 and 5, respectively. METHODOLOGY/PRINCIPAL
findingsIn the present study, we investigated in vitro the role of these same TLR and ligands, in alveolar macrophage (AM) and epithelial cell (EC) activation. Cellular responses to P. aeruginosa was evaluated by measuring KC, TNF-alpha, IL-6 and G-CSF secretion, four different markers of the innate immune response. AM and EC from WT and TLR2, 4, 5 and MyD88 knockout mice for were stimulated with the wild-type P. aeruginosa or with a mutant devoid of flagellin production. CONCLUSIONS/SIGNIFICANCE: The results clearly demonstrate that only two ligand/receptor pairs are necessary for the induction of KC, TNF-alpha, and IL-6 synthesis by P. aeruginosa-activated cells, i.e. TLR2,4/LPS and TLR5/flagellin. Either ligand/receptor pair is sufficient to sense the bacterium and to trigger cell activation, and when both are missing lung EC and AM are unable to produce such a response as were cells from MyD88(-/-) mice.
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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.