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A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Chorioamnionitis, postnatal factors and proinflammatory response in the pathogenetic sequence of bronchopulmonary
1University Children's Hospital, Würzburg, Germany. speer_c@kinderklinik.uni-wuerzburg.de
Insights
Pulmonary inflammation, driven by various factors, is key in bronchopulmonary dysplasia pathogenesis. This lung injury involves inflammatory cells, mediators, and impaired repair, impacting infant development.
Area of Science:
- Neonatal Medicine
- Pediatric Pulmonology
- Developmental Biology
Background:
- Bronchopulmonary dysplasia (BPD) is a complex lung disease in premature infants.
- Its pathogenesis involves multifactorial pre- and postnatal insults.
- Pulmonary inflammation is a central mechanism in BPD development.
Purpose of the Study:
- To elucidate the role of pulmonary inflammation in bronchopulmonary dysplasia.
- To identify key factors contributing to lung injury in premature infants.
- To understand the impact of inflammation on lung development in BPD.
Main Methods:
- Review of pre- and postnatal factors contributing to BPD.
- Analysis of inflammatory processes in the airways and lung tissue.
- Examination of mediators and cellular components involved in lung injury.
- Assessment of tissue remodeling and growth factor generation.
Main Results:
- Pre- and postnatal factors (e.g., chorioamnionitis, oxygen toxicity, ventilation, infection) induce inflammation.
- Inflammation involves inflammatory cell accumulation and proinflammatory mediators.
- An imbalance favoring proinflammatory factors is a hallmark of lung injury.
- Impaired repair and reduced growth factors affect alveolarization and vascular development.
Conclusions:
- Pulmonary inflammation is a critical component of bronchopulmonary dysplasia pathogenesis.
- Inflammatory insults and impaired repair mechanisms lead to long-term consequences for affected infants.
- Understanding these inflammatory pathways is crucial for developing therapeutic strategies for BPD.
Abstract:
Pulmonary inflammation has a central role in the multifactorial and complex pathogenesis of bronchopulmonary dysplasia. Pre- and postnatal factors such as chorioamnionitis, oxygen toxicity, mechanical ventilation and postnatal infections can induce and perpetuate an injurious and complex inflammatory response in the airways and lung tissue of very immature infants. This inflammatory process is characterized by the accumulation of inflammatory cells and an arsenal of proinflammatory mediators such as cytokines, toxic oxygen radicals, lipid mediators and potent proteases. An imbalance between pro- and anti-inflammatory factors favoring the proinflammatory process can be considered as a hallmark of lung injury. In addition, impaired mechanisms of tissue remodeling and repair together with a subnormal generation of growth factors could affect alveolarization and vascular development with lifelong consequences for the infants with bronchopulmonary dysplasia.
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