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

Poster (konferens)
Författare Maija Bry
Anna Hogmalm
Kristina Bry
Publicerad i Pediatric Academic Societies Annual Meeting
Publiceringsår 2015
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Språk en
Ämneskategorier Annan medicinsk grundvetenskap

Sammanfattning

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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