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Pre and Postnatal Inflammation in the Pathogenesis of Bronchopulmonary Dysplasia

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Bronchopulmonary Dysplasia

Part of the book series: Respiratory Medicine ((RM))

Abstract

Pathogenesis of bronchopulmonary dysplasia (BPD) is most likely multifactorial, and involvement of different pathogenetic mechanisms might lead to severe, mild, or moderate disease. BPD is characterized by inflammation, apoptosis, and extensive extracellular matrix remodeling. Pre and postnatal injurious conditions, such as chorioamnionitis, neonatal infection, hyperoxia, hypoxia, or mechanical ventilation have been shown to contribute to the onset and perpetuation of an inflammatory response in the functionally and structurally immature lungs of preterm infants. Perturbation of pro- and anti-inflammatory central signaling pathways and subsequently imbalanced inflammatory responses may lead to aberrant airway-branching and impaired development of epithelial, mesenchymal, and endothelial structures, seriously affecting lung development during a window of vulnerability in genetically susceptible infants. Alterations of normal alveolarization and pulmonary vascular development may result in lifelong impairment of lung function.

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Glaser, K., Speer, C.P. (2016). Pre and Postnatal Inflammation in the Pathogenesis of Bronchopulmonary Dysplasia. In: Bhandari, V. (eds) Bronchopulmonary Dysplasia. Respiratory Medicine. Humana Press, Cham. https://doi.org/10.1007/978-3-319-28486-6_3

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