ArticleJournal of immunology (Baltimore, Md. : 1950)2010
The inflammasome mediates hyperoxia-induced alveolar cell permeability.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 91 citations in OpenAlex.
- Diet-induced obesity alleviates epithelial damage in hyperoxic acute lung injury (HALI) in mice.Respiratory research · 2026Article
- Heart-Lung Interactions in Gas Exchange: From Physiology to Pathophysiology.Comprehensive Physiology · 2026Review
- Oxygen therapy enhances the systemic inflammatory response in a human model of experimental inflammation.International journal of cardiology. Heart & vasculature · 2026Article
- Gas6 induces AIM to suppress acute lung injury in mice by inhibiting NLRP3 inflammasome activation and inducing autophagy.Frontiers in immunology · 2025Article
- Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.Frontiers in physiology · 2025Article
- Pulmonary inflammation and viral replication define distinct clinical outcomes in fatal cases of COVID-19.PLoS pathogens · 2024Article
- Article
- Purinergic P2X7 receptor mediates hyperoxia-induced injury in pulmonary microvascular endothelial cells via NLRP3-mediated pyroptotic pathway.Open medicine (Warsaw, Poland) · 2024Article
- Modelling lung diffusion-perfusion limitation in mechanically ventilated SARS-CoV-2 patients.Frontiers in physiology · 2024Article
- Alveolar Hyperoxia and Exacerbation of Lung Injury in Critically Ill SARS-CoV-2 Pneumonia.Medical sciences (Basel, Switzerland) · 2023Review
- Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries.Antioxidants (Basel, Switzerland) · 2023Review
- A-Kinase Anchor Protein 1 deficiency causes mitochondrial dysfunction in mouse model of hyperoxia induced acute lung injury.Frontiers in pharmacology · 2022Article
- Glibenclamide Alleviates LPS-Induced Acute Lung Injury through NLRP3 Inflammasome Signaling Pathway.Mediators of inflammation · 2022Article
- Mitochondrial ProteinFrontiers in pharmacology · 2022Article
- BMI1 Silencing Induces Mitochondrial Dysfunction in Lung Epithelial Cells Exposed to Hyperoxia.Frontiers in physiology · 2022Article
- New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis.International journal of molecular sciences · 2021Review
- The pentose phosphate pathway mediates hyperoxia-induced lung vascular dysgenesis and alveolar simplification in neonates.JCI insight · 2021Article
- Pulmonary Interstitial Matrix and Lung Fluid Balance From Normal to the Acutely Injured Lung.Frontiers in physiology · 2021Review
- The α7 nicotinic acetylcholine receptor agonist, GTS-21, attenuates hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation.Molecular medicine (Cambridge, Mass.) · 2020Article
- Apoptosis signal-regulating kinase-1 promotes inflammasome priming in macrophages.American journal of physiology. Lung cellular and molecular physiology · 2019Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A hallmark of hyperoxic acute lung injury is the influx of inflammatory cells to lung tissue and the production of proinflammatory cytokines, such as IL-1beta; however, the mechanisms connecting hyperoxia and the inflammatory response to lung damage is not clear. The inflammasome protein complex activates caspase-1 to promote the processing and secretion of proinflammatory cytokines. We hypothesized that hyperoxia-induced K(+) efflux activates the inflammasome via the purinergic P2X7 receptor to cause inflammation and hyperoxic acute lung injury. To test this hypothesis, we characterized the expression and activation of inflammasome components in primary murine alveolar macrophages exposed to hyperoxia (95% oxygen and 5% CO(2)) in vitro, and in alveolar macrophages isolated from mice exposed to hyperoxia (100% oxygen). Our results showed that hyperoxia increased K(+) efflux, inflammasome formation, release of proinflammatory cytokines, and induction of caspase-1 and IL-1beta cleavage both in vitro and in vivo. The P2X7 agonist ATP enhanced hyperoxia-induced inflammasome activation, whereas the P2X7 antagonist, oxidized ATP, inhibited hyperoxia induced inflammasome activation. In addition, when ATP was scavenged with apyrase, hyperoxia-induced inflammasome activation was significantly decreased. Furthermore, short hairpin RNA silencing of inflammasome components abrogated hyperoxia-induced secretion of proinflammatory cytokines in vitro. These results suggest that hyperoxia induces K(+) efflux through the P2X7 receptor, leading to inflammasome activation and secretion of proinflammatory cytokines. These events would affect the permeability of the alveolar epithelium and ultimately lead to epithelial barrier dysfunction and cell death.
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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.