ArticleAmerican journal of respiratory cell and molecular biology2014
The NLRP3 inflammasome is required for the development of hypoxemia in LPS/mechanical ventilation acute lung injury.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.
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Who cites it
89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 127 citations in OpenAlex.
- Associations of variants In the hexokinase 1 and interleukin 18 receptor regions with oxyhemoglobin saturation during sleep.PLoS genetics · 2019Pooled it
- An Unsettled Promise: The Newborn Piglet Model of Neonatal Acute Respiratory Distress Syndrome (NARDS). Physiologic Data and Systematic Review.Frontiers in physiology · 2019Pooled it
- Effect of Colchicine vs Standard Care on Cardiac and Inflammatory Biomarkers and Clinical Outcomes in Patients Hospitalized With Coronavirus Disease 2019: The GRECCO-19 Randomized Clinical Trial.JAMA network open · 2020Trial
- The pyruvate kinase activator etavopivat (FT-4202) limits pulmonary and systemic sequelae of sepsis in a mouse LPS model.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Circulating and Respiratory Biomarkers in Sepsis-Induced ARDS: Diagnostic and Prognostic Insights - A Narrative Review.Journal of inflammation research · 2026Review
- The NLRP3 inhibitor, MCC950, attenuates environmental pollutant PMCurrent research in toxicology · 2026Article
- Palmatine Attenuates Lipopolysaccharide-Induced Acute Lung Injury Via Suppression of NLRP3 Inflammasome Activation, Pyroptosis, and Metabolic Remodeling.Inflammation · 2025Article
- Acute lung injury: pathogenesis and treatment.Journal of translational medicine · 2025Review
- MCC950 Alleviates Fat Embolism-Induced Acute Respiratory Distress Syndrome Through Dual Modulation of NLRP3 Inflammasome and ERK Pathways.International journal of molecular sciences · 2025Article
- Hypothermia protects against ventilator-induced lung injury by limiting IL-1β release and NETs formation.eLife · 2025Article
- Hypothermia protects against ventilator-induced lung injury by limiting IL-1β release and NETs formation.bioRxiv : the preprint server for biology · 2025Article
- Review
- NLRP3 promotes inflammatory signaling and IL-1β cleavage in acute lung injury caused by cell wall extract of Lactobacillus casei.Communications biology · 2025Article
- Aerosol Inhalation of Luteolin-7-O-Glucuronide Exerts Anti-Inflammatory Effects by Inhibiting NLRP3 Inflammasome Activation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- COVID-19 and the impact on Alzheimer's disease pathology.Journal of neurochemistry · 2024Review
- Characterization of a small molecule inhibitor of the NLRP3 inflammasome and its potential use for acute lung injury.Bioorganic chemistry · 2024Article
- Pulmonary inflammation and viral replication define distinct clinical outcomes in fatal cases of COVID-19.PLoS pathogens · 2024Article
- Evaluation of interleukin-1 and interleukin-6 receptor antagonists in a murine model of acute lung injury.Experimental physiology · 2024Article
- Review
- Regulated Cell Death of Alveolar Macrophages in Acute Lung Inflammation: Current Knowledge and Perspectives.Journal of inflammation research · 2024Review
29 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
IL-1β is a potent proinflammatory cytokine that is implicated in the pathogenesis of acute respiratory distress syndrome. We hypothesized that LPS and mechanical ventilation (MV) together could lead to IL-1β secretion and the development of acute lung injury (ALI), and that this process would be dependent on caspase-1 and the nucleotide binding domain and leucine-rich repeat (NLR) pyrin domain containing 3 (NLRP3) inflammasome activation. The objectives of this study were to determine the specific role of IL-1β, caspase-1, and the NLRP3 inflammasome in a two-hit model of ALI due to LPS plus MV. We used a two-hit murine model of ALI in which both inhaled LPS and MV were required for the development of hypoxemia, pulmonary neutrophil infiltration, and alveolar leakage. Nlrp3-deficent and Casp1-deficient mice had significantly diminished IL-1β levels in bronchoalveolar lavage fluid, and were specifically protected from hypoxemia, despite similar alveolar neutrophil infiltration and leakage. The IL-1 receptor antagonist, Anakinra, significantly improved the specific development of hypoxemia without significant effects on neutrophil infiltration or alveolar leakage. MV resulted in increased bronchoalveolar lavage extracellular ATP and alveolar macrophage apoptosis as triggers of NLRP3 inflammasome activation. NLRP3 inflammasome activation and IL-1β production play a key role in ALI caused by the combination of LPS and MV, particularly in the hypoxemia associated with acute respiratory distress syndrome. Blocking IL-1 signaling in this model specifically ameliorates hypoxemia, without affecting neutrophil infiltration and alveolar leakage, disassociating these readouts of ALI. MV causes alveolar macrophage apoptosis, a key step in the activation of NLRP3 inflammasome and production of IL-1β.
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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.