ArticleProceedings of the National Academy of Sciences of the United States of America2013
Interleukin-1 receptor antagonist prevents murine bronchopulmonary dysplasia induced by perinatal inflammation and hyperoxia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 2 of them syntheses that pooled it.
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Who cites it
111 citing papers in PubMed, 2 syntheses or guidelines pooled it, 154 citations in OpenAlex.
- Clinical Pharmacokinetics and Pharmacodynamics of the IL-1 Receptor Antagonist Anakinra: A Systematic Review.Clinical pharmacokinetics · 2026Pooled it
- Systems-level insights into bronchopulmonary dysplasia from meta-analysis of genome-scale studies.Respiratory research · 2026Pooled it
- Anakinra Pilot - a clinical trial to demonstrate safety, feasibility and pharmacokinetics of interleukin 1 receptor antagonist in preterm infants.Frontiers in immunology · 2022Trial
- Model-Informed Dose Optimization of Anakinra in Preterm Neonates Implications for Safe and Effective Dosing.Clinical pharmacology and therapeutics · 2026Article
- Bronchopulmonary dysplasia and prematurity-associated lung disease: emerging therapies to improve lifelong respiratory outcomes.European journal of pediatrics · 2026Review
- Cytokine multimerization: when more is more and sometimes less.Nature reviews. Immunology · 2026Review
- Bronchopulmonary Dysplasia and Innate Immunity: A Narrative Review of the Roles of IL-1β and IL-8 (CXCL8).Children (Basel, Switzerland) · 2026Review
- Anakinra in a Preterm Infant with Bronchopulmonary Dysplasia: A Case Report.Children (Basel, Switzerland) · 2026Article
- Umbilical cord blood cell transcriptional and methylation signatures at birth are associated with BPD development and chorioamnionitis: a pilot study.Scientific reports · 2026Article
- Predictive value of increased C-reactive protein levels in preterm infants on respiratory function at five to six years of age.Communications medicine · 2026Article
- PKM2 Promotes Glycolysis in Alveolar Macrophages and Induces Inflammation in Bronchopulmonary Dysplasia.Inflammation · 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
- The evolving pathophysiology of bronchopulmonary dysplasia.Physiological reviews · 2026Review
- Inflammatory mechanisms contribute to long-term cognitive deficits induced by perinatal asphyxia via interleukin-1.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Role of connexin 43 in hyperoxia-induced bronchopulmonary dysplasia and associated pulmonary hypertension.PloS one · 2026Article
- Pathogenesis of bronchopulmonary dysplasia: an immunological perspective.Frontiers in immunology · 2026Review
- Respiratory effects of off label anakinra in critically ill neonates: a 15-patient observational cohort study.Frontiers in pediatrics · 2026Article
- The Inflammatory Nexus of Bronchopulmonary Dysplasia: From Molecular Pathways to Precision Therapeutics.Mediators of inflammation · 2026Review
- Whole blood biophysical immune profiling of newborn infants correlates with immune responses.Pediatric research · 2025Article
- Umbilical Cord Blood Cell Transcriptional and Methylation Signatures at Birth Are Associated with BPD Development.bioRxiv : the preprint server for biology · 2025Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bronchopulmonary dysplasia (BPD) is a common lung disease of premature infants, with devastating short- and long-term consequences. The pathogenesis of BPD is multifactorial, but all triggers cause pulmonary inflammation. No therapy exists; therefore, we investigated whether the anti-inflammatory interleukin-1 receptor antagonist (IL-1Ra) prevents murine BPD. We precipitated BPD by perinatal inflammation (lipopolysaccharide injection to pregnant dams) and rearing pups in hyperoxia (65% or 85% O2). Pups were treated daily with IL-1Ra or vehicle for up to 28 d. Vehicle-injected animals in both levels of hyperoxia developed a severe BPD-like lung disease (alveolar number and gas exchange area decreased by up to 60%, alveolar size increased up to fourfold). IL-1Ra prevented this structural disintegration at 65%, but not 85% O2. Hyperoxia depleted pulmonary immune cells by 67%; however, extant macrophages and dendritic cells were hyperactivated, with CD11b and GR1 (Ly6G/C) highly expressed. IL-1Ra partially rescued the immune cell population in hyperoxia (doubling the viable cells), reduced the percentage that were activated by up to 63%, and abolished the unexpected persistence of IL-1α and IL-1β on day 28 in hyperoxia/vehicle-treated lungs. On day 3, perinatal inflammation and hyperoxia each triggered a distinct pulmonary immune response, with some proinflammatory mediators increasing up to 20-fold and some amenable to partial or complete reversal with IL-1Ra. In summary, our analysis reveals a pivotal role for IL-1α/β in murine BPD and an involvement for MIP (macrophage inflammatory protein)-1α and TREM (triggering receptor expressed on myeloid cells)-1. Because it effectively shields newborn mice from BPD, IL-1Ra emerges as a promising treatment for a currently irremediable disease that may potentially brighten the prognosis of the tiny preterm patients.
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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.