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Insulin-like growth factor-I (IGF-I) aggravates lung injury in a mouse model of bronchopulmonary dysplasia

Authors Maija Bry
Anna Hogmalm
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


Background: Trials using continuous intravenous administration of insulin-like growth factor (IGF)-I to preterm infants for the prevention of retinopathy of prematurity (ROP) are currently underway (Ley et al., 2013). However, the effects of exogenous IGF-I on developing organs of the newborn are unknown. IGF-I has been shown to play a critical role in the pathogenesis of asthma (Lee et al., 2014). In addition, IGF-I levels are high in the lungs of infants with bronchopulmonary dysplasia (BPD) (Capoluongo et al., 2008). We have previously shown that perinatal pulmonary IL-1b expression causes a BPD-like lung disease in newborn mice. Objective: To study the effects of systemic postnatal administration of IGF-I on lung inflammation and morphogenesis in a murine model of BPD. Methods: IL-1b production in pulmonary epithelium of transgenic fetuses and pups was induced by doxycycline administration (0.5 mg/ml) in drinking water to pregnant and lactating dams from the beginning of pregnancy until sacrifice of the pups on postnatal day (PN) 7. Three intraperitoneal injections of recombinant human IGF-I (1 μg/g body weight) or an equal volume of PBS were administered to transgenic IL-1β-expressing mice and their littermate controls on PN 2, 4 and 6. Lung inflammation and structure were studied on PN 7. Results: IGF-I significantly increased both neutrophil and macrophage infiltration in the lungs of IL-1b-expressing infant mice, and also significantly increased the number of neutrophils in the lungs of littermate controls not expressing IL-1β. In addition, IGF-I increased alveolar septal wall thickness in IL-1b-expressing mice, indicating that IGF-I potentiated IL-1b-induced lung injury. Conclusions: IGF-I aggravated lung inflammation and injury in the newborn lung, indicating that IGF-I administration may have deleterious effects on lung development in preterm infants at risk of BPD.

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