ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Absence of TNF-α enhances inflammatory response in the newborn lung undergoing mechanical ventilation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Association of TNF-α genetic variants with neonatal bronchopulmonary dysplasia: consolidated results.Frontiers in pediatrics · 2024Pooled it
- Maternal and Early Neonatal Serum Cytokine and Endothelin-1 Concentrations in Preeclampsia: A Single-Center Observational Cohort Study.Children (Basel, Switzerland) · 2026Article
- Preventive application of lung growth factors and lack of attenuation of phenotype disruption of lung resident MSC from preterm infants by hyperoxia.Molecular and cellular pediatrics · 2026Article
- Th1 differentiation and function are inhibited in neonates following human metapneumovirus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Mitochondria as the central regulator of cell death in bronchopulmonary dysplasia.Frontiers in physiology · 2025Review
- Senescence of lung mesenchymal stem cells of preterm infants by cyclic stretch and hyperoxia via p21.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Anti-CCL2 therapy reduces oxygen toxicity to the immature lung.Cell death discovery · 2024Article
- Molsidomine decreases hyperoxia-induced lung injury in neonatal rats.Pediatric research · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Complex roles of TGF-β signaling pathways in lung development and bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Molecular mechanisms of cell death in bronchopulmonary dysplasia.Apoptosis : an international journal on programmed cell death · 2023Review
- Mesenchymal stromal/stem cells and bronchopulmonary dysplasia.Frontiers in cell and developmental biology · 2023Review
- Insights into the Black Box of Intra-Amniotic Infection and Its Impact on the Premature Lung: From Clinical and Preclinical Perspectives.International journal of molecular sciences · 2022Review
- Association of immune cell recruitment and BPD development.Molecular and cellular pediatrics · 2022Review
- TRAIL protects the immature lung from hyperoxic injury.Cell death & disease · 2022Article
- When inflammation meets lung development-an update on the pathogenesis of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2022Review
- Oxygen Toxicity to the Immature Lung-Part I: Pathomechanistic Understanding and Preclinical Perspectives.International journal of molecular sciences · 2021Review
- Oxygen Toxicity to the Immature Lung-Part II: The Unmet Clinical Need for Causal Therapy.International journal of molecular sciences · 2021Review
- MSC Based Therapies to Prevent or Treat BPD-A Narrative Review on Advances and Ongoing Challenges.International journal of molecular sciences · 2021Review
- Integrative Studies of Human Cord Blood Derived Mononuclear Cells and Umbilical Cord Derived Mesenchyme Stem Cells in Ameliorating Bronchopulmonary Dysplasia.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Bronchopulmonary dysplasia (BPD), characterized by impaired alveolarization and vascularization in association with lung inflammation and apoptosis, often occurs after mechanical ventilation with oxygen-rich gas (MV-O2). As heightened expression of the proinflammatory cytokine TNF-α has been described in infants with BPD, we hypothesized that absence of TNF-α would reduce pulmonary inflammation, and attenuate structural changes in newborn mice undergoing MV-O2 Neonatal TNF-α null (TNF-α(-/-)) and wild type (TNF-α(+/+)) mice received MV-O2 for 8 h; controls spontaneously breathed 40% O2 Histologic, mRNA, and protein analysis in vivo were complemented by in vitro studies subjecting primary pulmonary myofibroblasts to mechanical stretch. Finally, TNF-α level in tracheal aspirates from preterm infants were determined by ELISA. Although MV-O2 induced larger and fewer alveoli in both, TNF-α(-/-) and TNF-α(+/+) mice, it caused enhanced lung apoptosis (TUNEL, caspase-3/-6/-8), infiltration of macrophages and neutrophils, and proinflammatory mediator expression (IL-1β, CXCL-1, MCP-1) in TNF-α(-/-) mice. These differences were associated with increased pulmonary transforming growth factor-β (TGF-β) signaling, decreased TGF-β inhibitor SMAD-7 expression, and reduced pulmonary NF-κB activity in ventilated TNF-α(-/-) mice. Preterm infants who went on to develop BPD showed significantly lower TNF-α levels at birth. Our results suggest a critical balance between TNF-α and TGF-β signaling in the developing lung, and underscore the critical importance of these key pathways in the pathogenesis of BPD. Future treatment strategies need to weigh the potential benefits of inhibiting pathologic cytokine expression against the potential of altering key developmental pathways.
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Registered trials
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