ArticleJCI insight2020
Prenatal inflammation enhances antenatal corticosteroid-induced fetal lung maturation.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 22 citations in OpenAlex.
- A single-cell transcriptomic atlas of the pigtail macaque placenta in late gestation.BMC genomics · 2026Article
- Phenotypes of Preterm Birth: A Retrospective Cohort Study from a Tertiary Romanian Centre as a Framework for Future Genomic and Proteomic Research.Journal of clinical medicine · 2026Article
- Evolutionary Integration and Glucocorticoid Regulation of the Respiratory System: Structure, Function, and Homeostatic Adaptation.Medical sciences (Basel, Switzerland) · 2026Review
- Decreased Glucocorticoid Receptor Expression and Function in Cord Blood Immune Cells from Preterm Neonates with Morbidity.International journal of molecular sciences · 2025Article
- Realistic expectations for changes to average human lifespan in the near future.Biogerontology · 2025Article
- The lung microvasculature promotes alveolar type 2 cell differentiation via secreted SPARCL1.Stem cell reports · 2025Article
- Perinatal glucocorticoid sensitivity in the preterm newborn: molecular mechanisms, endogenous determinants, and clinical implications.Frontiers in endocrinology · 2025Review
- Is there a role for early postnatal steroids in very preterm infants exposed to chorioamnionitis?Pediatric research · 2024Article
- Amnion responses to intrauterine inflammation and effects of inhibition of TNF signaling in preterm Rhesus macaque.iScience · 2023Article
- Empagliflozin improves kidney senescence induced by D-galactose by reducing sirt1-mediated oxidative stress.Biogerontology · 2023Article
- c-Myc Drives inflammation of the maternal-fetal interface, and neonatal lung remodeling induced by intra-amniotic inflammation.Frontiers in cell and developmental biology · 2023Article
- Understanding the role of placental pathophysiology in the development of bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2022Review
- Fetal maturation revealed by amniotic fluid cell-free transcriptome in rhesus macaques.JCI insight · 2022Article
- Placental dysfunction influences fetal monocyte subpopulation gene expression in preterm birth.JCI insight · 2022Article
- Inflammatory blockade prevents injury to the developing pulmonary gas exchange surface in preterm primates.Science translational medicine · 2022Article
- Review
- Sex-Specific Differences in MicroRNA Expression During Human Fetal Lung Development.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Respiratory complicˆations are the major cause of morbidity and mortality among preterm infants, which is partially prevented by the administration of antenatal corticosteroids (ACS). Most very preterm infants are exposed to chorioamnionitis, but short- and long-term effects of ACS treatment in this setting are not well defined. In low-resource settings, ACS increased neonatal mortality by perhaps increasing infection. We report that treatment with low-dose ACS in the setting of inflammation induced by intraamniotic lipopolysaccharide (LPS) in rhesus macaques improves lung compliance and increases surfactant production relative to either exposure alone. RNA sequencing shows that these changes are mediated by suppression of proliferation and induction of mesenchymal cellular death via TP53. The combined exposure results in a mature-like transcriptomic profile with inhibition of extracellular matrix development by suppression of collagen genes COL1A1, COL1A2, and COL3A1 and regulators of lung development FGF9 and FGF10. ACS and inflammation also suppressed signature genes associated with proliferative mesenchymal progenitors similar to the term gestation lung. Treatment with ACS in the setting of inflammation may result in early respiratory advantage to preterm infants, but this advantage may come at a risk of abnormal extracellular matrix development, which may be associated with increased risk of chronic lung disease.
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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.