ArticleProceedings of the National Academy of Sciences of the United States of America2002
CFTR is a pattern recognition molecule that extracts Pseudomonas aeruginosa LPS from the outer membrane into epithelial cells and activates NF-kappa B translocation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.
- Molecular exploration of host-pathogen interactions in severeFrontiers in medicine · 2025Pooled it
- Steering the course: targeting and exploiting surface receptors in phage therapy.Journal of bacteriology · 2026Review
- Lipopolysaccharide Causes Acquired CFTR Dysfunction in Murine Nasal Airways.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2025Article
- An Antibiotic Nanobomb Constructed from pH-Responsive Chemical Bonds in Metal-Phenolic Network Nanoparticles for Biofilm Eradication and Corneal Ulcer Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Reduced Sphingosine in Cystic Fibrosis Increases Susceptibility toInternational journal of molecular sciences · 2023Article
- Article
- Current concepts on Pseudomonas aeruginosa interaction with human airway epithelium.PLoS pathogens · 2023Review
- Pseudomonas aeruginosa in the Cystic Fibrosis Lung.Advances in experimental medicine and biology · 2022Article
- Article
- Analysis of the Structure and Biosynthesis of the Lipopolysaccharide Core Oligosaccharide ofInternational journal of molecular sciences · 2021Article
- The lipopolysaccharide outer core transferase genes pcgD and hptE contribute differently to the virulence of Pasteurella multocida in ducks.Veterinary research · 2021Article
- Airway Inflammation and Host Responses in the Era of CFTR Modulators.International journal of molecular sciences · 2020Review
- The Role ofPathogens (Basel, Switzerland) · 2019Review
- Repression of eEF2K transcription by NF-κB tunes translation elongation to inflammation and dsDNA-sensing.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Targeting host lipid flows: Exploring new antiviral and antibiotic strategies.Cellular microbiology · 2019Review
- Microbial uptake by the respiratory epithelium: outcomes for host and pathogen.FEMS microbiology reviews · 2019Review
- Pathogenomics of Virulence Traits ofFrontiers in microbiology · 2018Article
- Ion channels of the lung and their role in disease pathogenesis.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Lipopolysaccharide modification in Gram-negative bacteria during chronic infection.FEMS microbiology reviews · 2016Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Immune cells are activated during cellular responses to antigen by two described mechanisms: (i) direct uptake of antigen and (ii) extraction and internalization of membrane components from antigen-presenting cells. Although endocytosis of microbial antigens by pattern recognition molecules (PRM) also activates innate immunity, it is not known whether this involves extraction and internalization of microbial surface components. Epithelial cells on mucosal surfaces use a variety of receptors that are distinct from the classical endocytic PRM to bind and internalize intact microorganisms. Nonclassical receptor molecules theoretically could act as a type of endocytic PRM if these molecules could recognize, bind, extract, and internalize a pathogen-associated molecule and initiate cell signaling. We report here that the interaction between the cystic fibrosis transmembrane conductance regulator (CFTR) and the outer core oligosaccharide of the lipopolysaccharide (LPS) in the outer membrane of Pseudomonas aeruginosa satisfies all of these conditions. P. aeruginosa LPS was specifically recognized and bound by CFTR, extracted from the organism's surface, and endocytosed by epithelial cells, leading to a rapid (5- to 15-min) and dynamic translocation of nuclear transcription factor NF-kappa B. Inhibition of epithelial cell internalization of P. aeruginosa LPS prevented NF-kappa B activation. Cellular activation depended on expression of wild-type CFTR, because both cultured Delta F508 CFTR human airway epithelial cells and lung epithelial cells of transgenic-CF mice failed to endocytose LPS and translocate NF-kappa B. CFTR serves as a critical endocytic PRM in the lung epithelium, coordinating the effective innate immune response to P. aeruginosa infection.
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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.