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Mechanisms of inflammatory lung injury in the neonate: lessons from a transgenic mouse model of bronchopulmonary dysplasia.

Review article
Authors Kristina Bry
Anna Hogmalm
Erica Bäckström
Published in Seminars in perinatology
Volume 34
Issue 3
Pages 211-21
ISSN 1558-075X
Publication year 2010
Published at Institute of Clinical Sciences, Department of Pediatrics
Pages 211-21
Language en
Keywords Airway Remodeling, Animals, Animals, Newborn, Bronchopulmonary Dysplasia, pathology, physiopathology, Chorioamnionitis, physiopathology, Female, Humans, Infant, Newborn, Inflammation, Integrin beta Chains, physiology, Interleukin-1beta, physiology, Lung, pathology, Matrix Metalloproteinase 9, physiology, Mice, Mice, Transgenic, Pregnancy, Premature Birth, etiology, Transforming Growth Factor beta1, physiology
Subject categories Pediatrics


The role of inflammation in the pathogenesis of bronchopulmonary dysplasia (BPD) is not well understood. By using a transgenic mouse expressing the inflammatory cytokine interleukin (IL)-1beta in the lung, we have shown that perinatal expression of IL-1beta causes a BPD-like illness in infant mice. We have used this model to identify mechanisms by which inflammation causes neonatal lung injury. Increased matrix metalloproteinase (MMP)-9 activity is associated with BPD. MMP-9 deficiency worsens alveolar hypoplasia in IL-1beta-expressing newborn mice, suggesting that MMP-9 has a protective role in neonatal inflammatory lung injury. The beta6 integrin subunit, an activator of transforming growth factor-beta, is involved in adult lung disease. Absence of the beta6 integrin subunit improves alveolar development in IL-1beta-expressing mice, suggesting that the beta6 integrin subunit is a pathogenetic factor in inflammatory lung disease in the newborn. The authors of clinical studies who have examined maternal inflammation as a risk factor for BPD have found variable results. We have shown that maternal IL-1beta production preceding fetal IL-1beta production prevents lung inflammation, alveolar hypoplasia, and airway remodeling in newborn IL-1beta-expressing mice. Thus, maternal inflammation may protect the newborn lung against subsequent inflammatory injury. In contrast, when maternal and fetal production of IL-1beta are induced simultaneously, the development of IL-1beta-induced lung disease in the newborn is not prevented.

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