ArticleNature communications2015
The NLRP3 inflammasome is critically involved in the development of bronchopulmonary dysplasia.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 2 of them syntheses that pooled it.
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Who cites it
120 citing papers in PubMed, 2 syntheses or guidelines pooled it, 179 citations in OpenAlex.
- An Unsettled Promise: The Newborn Piglet Model of Neonatal Acute Respiratory Distress Syndrome (NARDS). Physiologic Data and Systematic Review.Frontiers in physiology · 2019Pooled it
- Meta-Analysis of Maternal and Fetal Transcriptomic Data Elucidates the Role of Adaptive and Innate Immunity in Preterm Birth.Frontiers in immunology · 2018Pooled it
- HSP90 Inhibitor, AT13387 Mitigates Chronic Lung Injury in Pre-Pubertal Mice: A Therapeutic Axis in Bronchopulmonary Dysplasia.Biomolecules · 2026Article
- Mesenchyme-derived inflammation during the saccular stage recruits macrophages and alters lung development.JCI insight · 2026Article
- Bronchopulmonary Dysplasia and Innate Immunity: A Narrative Review of the Roles of IL-1β and IL-8 (CXCL8).Children (Basel, Switzerland) · 2026Review
- The 20-HETE/GPR75 Axis Drives NLRP1 Inflammasome Activation via p53 in Bronchopulmonary Dysplasia.Advanced biology · 2026Article
- The autonomic nervous system-lung interface in experimental BPD: NPY modulates immune response, alveolar growth and vascular muscularizationin neonatal mice exposed to oxidative stress.Respiratory research · 2026Article
- Tracheal aspirates of mechanically ventilated preterm infants possess cytopathic tau variants: a prospective exploratory study.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- 1,25(OH)₂D₃ mitigates bronchopulmonary dysplasia via modulation of the TXNIP-NLRP3-GSDMD signaling pathway.Molecular biology reports · 2026Article
- Anakinra in a Preterm Infant with Bronchopulmonary Dysplasia: A Case Report.Children (Basel, Switzerland) · 2026Article
- Caffeine inhibited the hyperoxia-induced A2AR-ERK/p38 MAPK-IL-8 pathway in type II alveolar epithelial cells to suppress NETs formation in bronchopulmonary dysplasia.Pediatric research · 2026Article
- Review on the Mechanism of and Therapies Targeting PANoptosis in Ulcerative Colitis.Biomolecules · 2026Review
- Article
- Betaine improves hyperoxic lung injury through downregulating pulmonary macrophage pyroptosis in newborn mice.Pediatric research · 2026Article
- Dynamic association between plasma interleukin-1 family concentrations and bronchopulmonary dysplasia in extremely premature infants.Journal of perinatology : official journal of the California Perinatal Association · 2026Article
- In silico drug discovery and molecular dynamics simulation for targeting neonatal pneumonia and bronchopulmonary dysplasia.Frontiers in chemistry · 2026Article
- The evolving pathophysiology of bronchopulmonary dysplasia.Physiological reviews · 2026Review
- Pathogenesis of bronchopulmonary dysplasia: an immunological perspective.Frontiers in immunology · 2026Review
- The Inflammatory Nexus of Bronchopulmonary Dysplasia: From Molecular Pathways to Precision Therapeutics.Mediators of inflammation · 2026Review
- Reduced NLRP3, AIM2 and NLRC4 inflammasome activity in cord blood of extremely preterm infants.Frontiers in pediatrics · 2026Article
60 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
10 authors at 3 institutions in 1 country.
Funding
Abstract
The pathogenesis of bronchopulmonary dysplasia (BPD), a devastating lung disease in preterm infants, includes inflammation, the mechanisms of which are not fully characterized. Here we report that the activation of the NLRP3 inflammasome is associated with the development of BPD. Hyperoxia-exposed neonatal mice have increased caspase-1 activation, IL1β and inflammation, and decreased alveolarization. Nlrp3(-/-) mice have no caspase-1 activity, no IL1β, no inflammatory response and undergo normal alveolarization. Treatment of hyperoxia-exposed mice with either IL1 receptor antagonist to block IL1β or glyburide to block the Nlrp3 inflammasome results in decreased inflammation and increased alveolarization. Ventilated preterm baboons show activation of the NLRP3 inflammasome with increased IL1β:IL1ra ratio. The IL1β:IL1ra ratio in tracheal aspirates from preterm infants with respiratory failure is predictive of the development of BPD. We conclude that early activation of the NLRP3 inflammasome is a key mechanism in the development of BPD, and represents a novel therapeutic target for BPD.
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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.