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Mol Cell Pediatr. 2016 Dec;3(1):23. doi: 10.1186/s40348-016-0051-9. Epub 2016 Jun 29.

Pathogenesis of bronchopulmonary dysplasia: when inflammation meets organ development.

Author information

1
1Department of General Pediatrics and Neonatology, Center for Pediatrics and Youth Medicine, Justus-Liebig-University, Feulgenstrasse 12, D-35392 Gießen, Universities of Gießen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Giessen, Germany.
2
University of Giessen Lung Center, Excellence Cluster Cardio-Pulmonary Systems, Member of the German Lung Center, Department of Internal Medicine II, Aulweg 130, 35392, Giessen, Germany.
3
1Department of General Pediatrics and Neonatology, Center for Pediatrics and Youth Medicine, Justus-Liebig-University, Feulgenstrasse 12, D-35392 Gießen, Universities of Gießen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Giessen, Germany. Harald.Ehrhardt@paediat.med.uni-giessen.de.
4
University of Giessen Lung Center, Excellence Cluster Cardio-Pulmonary Systems, Member of the German Lung Center, Department of Internal Medicine II, Aulweg 130, 35392, Giessen, Germany. Harald.Ehrhardt@paediat.med.uni-giessen.de.

Abstract

Bronchopulmonary dysplasia is a chronic lung disease of preterm infants. It is caused by the disturbance of physiologic lung development mainly in the saccular stage with lifelong restrictions of pulmonary function and an increased risk of abnormal somatic and psychomotor development. The contributors to this disease's entity are multifactorial with pre- and postnatal origin. Central to the pathogenesis of bronchopulmonary is the induction of a massive pulmonary inflammatory response due to mechanical ventilation and oxygen toxicity. The extent of the pro-inflammatory reaction and the disturbance of further alveolar growth and vasculogenesis vary largely and can be modified by prenatal infections, antenatal steroids, and surfactant application.This minireview summarizes the important recent research findings on the pulmonary inflammatory reaction obtained in patient cohorts and in experimental models. Unfortunately, recent changes in clinical practice based on these findings had only limited impact on the incidence of bronchopulmonary dysplasia.

KEYWORDS:

Alveologenesis; Antenatal steroids; Apoptosis; Bronchopulmonary dysplasia; Chronic lung disease of the preterm infant; Infection; Inflammation; Lung development; Surfactant; Vasculogenesis

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