Grant: Project Grant

Treatments related to preterm birth and bronchopulmonary dysplasia (BPD) exert important financial constraints on the healthcare system. BPD is a disease arising as a consequence of preterm birth affecting lung structures. The subject of this research is based on the essential role of sex steroids in lung development. Many cells, not involved in sexual characteristics, use a sex steroid precursor (SSP) from blood to produce sex steroids specifically for themselves. DHEA, an important human SSP, is produced at high levels by the placenta late in gestation in such a way that most of the babies born preterm are deprived of this high level of SSP. We have shown recently in the mouse that the production of androgens within the lung from a blood SSP is essential to normal lung development of males and females and also reduces lung damages observed upon laboratory-induced BPD. Our hypothesis is that administration of SSP to preterm neonates will reduce morbidity associated with preterm birth and will reduce the severity of BPD. To test this hypothesis, SSP will be administered to preterm mice with and without laboratory-induced BPD consisting in a 3-day exposure of preterm newborns to a 80% oxygen atmosphere. The proposed research is a proof-of-concept aiming to demonstrate in a mouse model that SSP replacement therapy reduces preterm morbidity and reduces the severity of experimental BPD. SSP replacement therapy is a potential therapeutic avenue using an already available drug that may be rapidly tested in clinic settings.