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Postnatal lung inflammation leads to abnormal lung structure and function in adulthood

Authors Anna Hogmalm
Maija Bry
Kristina Bry
Published in Pediatric Academic Societies Annual Meeting
Publication year 2015
Published at Institute of Clinical Sciences, Department of Pediatrics
Language en
Subject categories Other Basic Medicine, Health Sciences


Background: Exposure to chorioamnionitis, mechanical ventilation, and the use of oxygen therapy cause inflammation in the preterm lung. The long-term consequences of neonatal pulmonary inflammation on lung structure and function have been incompletely characterized. We have previously shown that postnatal pulmonary IL-1b expression during the late saccular to alveolar stage of lung development causes lung inflammation and a mild increase in alveolar size and septal wall thickness in infant mice. Objective: To study the consequences of postnatal IL-1b expression in the newborn lung on lung structure and function in adulthood. Methods: To induce IL-1b production in the pulmonary epithelium of transgenic mice during the late saccular to alveolar stage of lung development, doxycycline (0.15 mg) was administered via intraperitoneal injections to transgenic pups and their littermate controls on postnatal days (PN) 0, 0.5, and 1. Lung inflammation, structure and airway reactivity (assessed by flexiVentTM at methacholine concentrations 0-200 mg/ml) were studied on PN 21 and 42. Results: IL-1b expression in the infant mice caused lack of alveolar septation in the lungs of young (PN 21) and adult (PN 42) mice (Fig. 2) and increased airway reactivity in the mice (Fig. 3). Conclusions: Postnatal lung inflammation in newborn mice caused abnormal lung structure and function in adulthood. Lack of alveolar septation in the newborn persisted after IL-1b production was stopped. Neonatal pulmonary inflammation thus has long-term consequences on the lung and may cause respiratory impairment in adulthood.

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