ArticleNature communications2023
NLRP3 selectively drives IL-1β secretion by Pseudomonas aeruginosa infected neutrophils and regulates corneal disease severity.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
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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
38 citing papers in PubMed, 64 citations in OpenAlex.
- Inflammasome Dynamics in the High-Risk Clone ST235 with Altered Pyoverdine Structures.International journal of molecular sciences · 2026Article
- Article
- Mechanisms underlying pyogenic bacterial infections of the skin.Archives of microbiology · 2026Review
- Comprehensive characterization of virulence factors in Pseudomonas aeruginosa clinical isolates from Bushehr, Iran: High proportion of exoU-positive isolates.BMC microbiology · 2026Article
- TH5487 specifically targets NLRP3 in FCAS patients resistant to MCC950.Communications biology · 2026Article
- Monosodium Glutamate InhibitsMicroorganisms · 2026Article
- NLRP10 engages oxidized DNA through a Schiff-base mechanism and dissociates from NLRP3 upon inflammasome activation.Communications biology · 2026Article
- Therapeutic Potential of Isoniazid in Inflammatory Skin Diseases: A Review.Clinical, cosmetic and investigational dermatology · 2026Review
- Mechanistic domains in canine corneal ulcer progression: a conceptual framework for adjunctive management.Frontiers in veterinary science · 2026Review
- Advances in loading-release-repair strategies of hydrogels for anterior segment disease therapy.Frontiers in immunology · 2026Review
- Immunoregulatory mechanisms in parasitic eosinophilic lung disease: the role of IgE immune complexes and NLRC4 inflammasome.Frontiers in immunology · 2026Review
- α-hemolysin polymorphisms in methicillin-resistantbioRxiv : the preprint server for biology · 2025Article
- Interplay between T3SS effectors, ExoY activation, and cGMP signaling in Pseudomonas aeruginosa infection.Nature communications · 2025Article
- Advances inMicroorganisms · 2025Review
- Neutrophil death-more than meets the eye.Experimental hematology · 2025Review
- A Synthetic Phage-Peptide Conjugate as a Potent Antibacterial Agent forACS central science · 2025Article
- Machine learning based screening of biomarkers associated with cell death and immunosuppression of multiple life stages sepsis populations.Scientific reports · 2025Article
- Inhibiting NLRP3 Inflammasome Activation to Alleviate Retinal Inflammation and Protect the Optic Nerve of OPTN(E50K)Mice.Inflammation · 2025Article
- EpithelialMedComm · 2025Article
- [Mechanisms of HNE mediated NLRP3 promoting EMT in chronic rhinosinusitis with polyps].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophages infected with Gram-negative bacteria expressing Type III secretion system (T3SS) activate the NLRC4 inflammasome, resulting in Gasdermin D (GSDMD)-dependent, but GSDME independent IL-1β secretion and pyroptosis. Here we examine inflammasome signaling in neutrophils infected with Pseudomonas aeruginosa strain PAO1 that expresses the T3SS effectors ExoS and ExoT. IL-1β secretion by neutrophils requires the T3SS needle and translocon proteins and GSDMD. In macrophages, PAO1 and mutants lacking ExoS and ExoT (ΔexoST) require NLRC4 for IL-1β secretion. While IL-1β release from ΔexoST infected neutrophils is also NLRC4-dependent, infection with PAO1 is instead NLRP3-dependent and driven by the ADP ribosyl transferase activity of ExoS. Genetic and pharmacologic approaches using MCC950 reveal that NLRP3 is also essential for bacterial killing and disease severity in a murine model of P. aeruginosa corneal infection (keratitis). Overall, these findings reveal a function for ExoS ADPRT in regulating inflammasome subtype usage in neutrophils versus macrophages and an unexpected role for NLRP3 in P. aeruginosa keratitis.
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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.