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Development of a Neonatal Piglet Acute Lung Injury Model Recreating the Early Environment of Preterm Infant Lungs
Published on: October 31, 2025
Pathogenesis of bronchopulmonary dysplasia
Patricia R Chess1, Carl T D'Angio, Gloria S Pryhuber
1Department of Pediatrics, University of Rochester, Rochester, NY 14642, USA. patricia_chess@urmc.rochester.edu
Insights
Bronchopulmonary dysplasia (BPD) in premature infants has evolved from a fibrotic endpoint to disordered lung development. Understanding new BPD involves factors like oxygen, ventilation, inflammation, and genetics.
Area of Science:
- Neonatology
- Pediatric Pulmonology
- Developmental Biology
Background:
- Bronchopulmonary dysplasia (BPD) initially presented as a fibrotic lung injury in premature infants following severe Respiratory Distress Syndrome (RDS).
- Advances in RDS treatment have altered the clinical presentation of BPD, shifting focus from fibrosis to impaired lung development.
- BPD remains a significant challenge, affecting thousands of premature infants annually.
Purpose of the Study:
- To summarize the multifaceted pathophysiologic factors contributing to the "new" BPD phenotype.
- To discuss the key elements driving disordered or delayed lung development in contemporary BPD cases.
Main Methods:
- Review and synthesis of existing literature on BPD pathogenesis.
- Discussion of various contributing factors including environmental, physiological, and genetic elements.
Main Results:
- The "new" BPD is characterized by abnormal lung development rather than fibrosis.
- Multiple factors including hyperoxia/hypoxia, mechanical ventilation, inflammation, PDA, nutrition, and genetics play crucial roles.
Conclusions:
- The evolving nature of BPD necessitates a comprehensive understanding of its complex pathophysiology.
- Addressing the "new" BPD requires a multi-pronged approach targeting its diverse contributing factors.
Abstract:
Bronchopulmonary dysplasia (BPD), initially described 40 years ago, is a dynamic clinical entity that continues to affect tens of thousands of premature infants each year. BPD was first characterized as a fibrotic pulmonary endpoint following severe Respiratory Distress Syndrome (RDS). It was the result of pulmonary healing after RDS, high oxygen exposure, positive pressure ventilation, and poor bronchial drainage secondary to endotracheal intubation in premature infants. With improved treatment for RDS, including surfactant replacement, oxygen saturation monitoring, improved modes of mechanical ventilation, antibiotic therapies, nutritional support, and infants surviving at younger gestations, the clinical picture of BPD has changed. In the following pages, we will summarize the multifaceted pathophysiologic factors leading to the pulmonary changes in "new" BPD, which is primarily characterized by disordered or delayed development. The contribution of hyperoxia and hypoxia, mechanical forces, vascular maldevelopment, inflammation, fluid management, patent ductus arteriosus (PDA), nutrition, and genetics will be discussed.
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