ArticleThe Journal of experimental medicine2007
Immune recognition of Pseudomonas aeruginosa mediated by the IPAF/NLRC4 inflammasome.
Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 309 papers.
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.
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Who cites it
309 citing papers in PubMed, 500 citations in OpenAlex.
- Innate immune sensors of inflammasomes and PANoptosomes: structural-mechanistic insights and therapeutic implications.Cell research · 2026Review
- Phosphoglycerate dehydrogenase-mediated serine reprogramming aggravates macrophage hyperinflammation in murine Pseudomonas aeruginosa pneumonia.Nature communications · 2026Article
- Targeting inflammasome, IL-1β, and coagulation in melioidosis.Frontiers in microbiology · 2026Review
- Toward precision host-directed immunomodulation in community-acquired pneumonia: a proposed endotype-target-natural-product framework and a roadmap for validation in human lung organoids.Frontiers in medicine · 2026Review
- Gastrointestinal microbiota and inflammasomes interplay in health and disease: a gut feeling.Gut · 2025Review
- Inflammasomes and pyroptosis in cancer: mechanisms and therapeutic advances.Journal of hematology & oncology · 2025Review
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Regulation of inflammatory processes by caspases.Nature reviews. Molecular cell biology · 2025Review
- 5-Methyluridine is Ubiquitous in Pseudomonas aeruginosa tRNA and Modulates Antimicrobial Resistance and Virulence.Journal of molecular biology · 2025Article
- Caspase-11 drives macrophage hyperinflammation in models of Polg-related mitochondrial disease.Nature communications · 2025Article
- Pyroptosis of pulmonary fibroblasts and macrophages through NLRC4 inflammasome leads to acute respiratory failure.Cell reports · 2025Article
- Pattern Recognition by NOD-Like Receptors.Advances in experimental medicine and biology · 2025Review
- The role of pyroptosis in cancer: key components and therapeutic potential.Cell communication and signaling : CCS · 2024Review
- NLRP3 inflammasome activity and periodontal disease pathogenesis-A bidirectional relationship.Oral diseases · 2024Review
- Pseudomonas aeruginosa Mediates Host Necroptosis through Rhl-Pqs Quorum Sensing Interaction.ImmunoHorizons · 2024Article
- The NLR family of innate immune and cell death sensors.Immunity · 2024Review
- Cytotoxic rhamnolipid micelles drive acute virulence inInfection and immunity · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Review
- Cytotoxic rhamnolipid micelles drive acute virulence inbioRxiv : the preprint server for biology · 2023Article
249 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
6 authors at 2 institutions in 1 country.
Funding
Abstract
Pseudomonas aeruginosa is a Gram-negative bacterium that causes opportunistic infections in immunocompromised individuals. P. aeruginosa employs a type III secretion system to inject effector molecules into the cytoplasm of the host cell. This interaction with the host cell leads to inflammatory responses that eventually result in cell death. We show that infection of macrophages with P. aeruginosa results in activation of caspase-1 in an IPAF-dependent, but flagellin-independent, manner. Macrophages deficient in IPAF or caspase-1 were markedly resistant to P. aeruginosa-induced cell death and release of the proinflammatory cytokine interleukin (IL)-1beta. A subset of P. aeruginosa isolates express the effector molecule exoenzyme U (ExoU), which we demonstrate is capable of inhibiting caspase-1-driven proinflammatory cytokine production. This study shows a key role for IPAF and capase-1 in innate immune responses to the pathogen P. aeruginosa, and also demonstrates that virulent ExoU-expressing strains of P. aeruginosa can circumvent this innate immune response.
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What OpenQuestion holds
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.