ArticleAmerican journal of physiology. Lung cellular and molecular physiology2019
Consequences of early postnatal lipopolysaccharide exposure on developing lungs in mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 47 citations in OpenAlex.
- Development of Versatile Nanoparticle System for Efficient Drug Delivery into Pulmonary Endothelium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Functional divergence of Capicua isoforms explains differential tissue vulnerability in neurological disease.Genes & development · 2026Article
- Bronchopulmonary dysplasia associated pulmonary hypertension: implications across the lifespan.Paediatric respiratory reviews · 2026Review
- Predictive value of increased C-reactive protein levels in preterm infants on respiratory function at five to six years of age.Communications medicine · 2026Article
- Reorienting catch-up growth research toward early-life prevention of metabolic disorders using natural products.Frontiers in endocrinology · 2026Article
- Targeting IL6-Edn1-FoxO1 axis enables lung growth in mechanically ventilated newborn mice.The European respiratory journal · 2025Article
- Adrenomedullin overexpression protects mice from experimental bronchopulmonary dysplasia and associated pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Dynamics of postnatal upper airway bacteria colonization in preterm infants <1000g and bronchopulmonary dysplasia.Scientific reports · 2025Article
- Functional divergence of Capicua isoforms explains differential tissue vulnerability in neurological disease.bioRxiv : the preprint server for biology · 2025Article
- Defining endotypes of bronchopulmonary dysplasia in preterm infants to improve precision-based therapies.JCI insight · 2025Review
- Proteomic analysis of premature umbilical cord blood and its relationship with bronchopulmonary dysplasia.Italian journal of pediatrics · 2025Observational
- Blocking IL-17a Signaling Decreases Lung Inflammation and Improves Alveolarization in Experimental Bronchopulmonary Dysplasia.The American journal of pathology · 2024Article
- The Human Microbiome-A Physiologic Perspective.Comprehensive Physiology · 2024Review
- Amphiregulin Exerts Proangiogenic Effects in Developing Murine Lungs.Antioxidants (Basel, Switzerland) · 2024Article
- Cord blood stem cell‑derived Angptl7 ameliorates the severity of bronchopulmonary dysplasia via anti‑inflammatory and proangiogenic effects.Molecular medicine reports · 2024Article
- Microbial signatures in amniotic fluid at preterm birth and association with bronchopulmonary dysplasia.Respiratory research · 2023Observational
- Bronchopulmonary Dysplasia: Pathogenesis and Pathophysiology.Journal of clinical medicine · 2023Review
- The SARS-CoV-2 E protein induces Toll-like receptor 2-mediated neonatal lung injury in a model of COVID-19 viremia that is rescued by the glucocorticoid ciclesonide.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Perinatal origins of bronchopulmonary dysplasia-deciphering normal and impaired lung development cell by cell.Molecular and cellular pediatrics · 2023Review
- Extracellular Signal-Regulated Kinase 1 Alone Is Dispensable for Hyperoxia-Mediated Alveolar and Pulmonary Vascular Simplification in Neonatal Mice.Antioxidants (Basel, Switzerland) · 2022Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Bronchopulmonary dysplasia (BPD) is a chronic lung disease of infants that is characterized by interrupted lung development. Postnatal sepsis causes BPD, yet the contributory mechanisms are unclear. To address this gap, studies have used lipopolysaccharide (LPS) during the alveolar phase of lung development. However, the lungs of infants who develop BPD are still in the saccular phase of development, and the effects of LPS during this phase are poorly characterized. We hypothesized that chronic LPS exposure during the saccular phase disrupts lung development by mechanisms that promote inflammation and prevent optimal lung development and repair. Wild-type C57BL6J mice were intraperitoneally administered 3, 6, or 10 mg/kg of LPS or a vehicle once daily on postnatal days (PNDs) 3-5. The lungs were collected for proteomic and genomic analyses and flow cytometric detection on PND6. The impact of LPS on lung development, cell proliferation, and apoptosis was determined on PND7. Finally, we determined differences in the LPS effects between the saccular and alveolar lungs. LPS decreased the survival and growth rate and lung development in a dose-dependent manner. These effects were associated with a decreased expression of proteins regulating cell proliferation and differentiation and increased expression of those mediating inflammation. While the lung macrophage population of LPS-treated mice increased, the T-regulatory cell population decreased. Furthermore, LPS-induced inflammatory and apoptotic response and interruption of cell proliferation and alveolarization was greater in alveolar than in saccular lungs. Collectively, the data support our hypothesis and reveal several potential therapeutic targets for sepsis-mediated BPD in infants.
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