459 - Circulating endothelial progenitor cells and the development of bronchopulmonary dysplasia in extremely preterm infants

Poster Number: 459
Publication Number: 459.432

Ashley Olszewski, University of Kentucky College of Medicine, Lexington, KY, United States; Peter J. Giannone, University of Kentucky College of Medicine, Lexington, KY, United States; John Bauer, University of Kentucky College of Medicine, Lexington, KY, United States; Hong Huang, University of Kentucky College of Medicine, Lexington, KY, United States; Brandon Schanbacher, university of kentucky, lexington, KY, United States; Aric Schadler, University of Kentucky College of Medicine, Lexington, KY, United States

Background: Bronchopulmonary dysplasia (BPD) disrupts alveolarization and pulmonary microvascular development in early lung development. Evidence supports the necessity of angiogenesis for normal lung development and circulating endothelial progenitor cells (EPCs) may be critical to the normal development of the pulmonary microvasculature and maintenance of lung structure after exposure to inflammation and injury. Damage or depletion of circulating EPCs after very preterm birth (at a critical period in lung development) may contribute to the pathogenesis of BPD.

Objective: We examined the relationship between changes in EPCs and BPD in premature infants ( < 30wks GA), testing the hypothesis that a lower proportion of proangiogenic circulating endothelial progenitor cells in the first week of life predicts the outcome of BPD.

Design/Methods: IRB approved retrospective cohort study of 216 premature infants. Circulating EPC data were collected prospectively from the umbilical cord blood, on NICU admission and DOL1,2,3,7,30,60. EPCs were counted via flow cytometry and defined as those with pro-angiogenic potential (CD133+/CD34+/CD45-). Antenatal and infant characteristics, respiratory data (surfactant, duration of respiratory support, supplemental oxygen) from birth to 36 weeks’ postmenstrual age, and discharge outcomes were determined. BPD was defined by the need for supplemental oxygen (FiO2 >0.21) at 36 weeks’ postmenstrual age.

Results: Significant differences in the proportion of CD133+/CD45- and AC133+/CD34+/CD45- cells in cord blood and on DOL 7 were observed between groups (no BPD vs BPD). Infants with BPD had a significantly higher proportion of proangiogenic circulating EPCs in cord blood compared to those with no BPD (CD45-/CD34+, p=0.0154; CD45-/AC133+/CD34+, p=0.026). On DOL 7, infants with BPD had a significantly lower proportion of proangiogenic circulating EPCs compared to those that do not develop BPD (CD34+/CD45- p =0.0318; CD133+/CD34+/ CD45-, p =0.038).Conclusion(s): In premature infants born before 30 weeks’ gestation there are fewer circulating endothelial cells on day of life 7 compared to cord blood. The decline in circulating endothelial progenitor cells over the first week of life was greater for infants that develop bronchopulmonary dysplasia. Understanding temporal changes in EPCs in early life may aid earlier identification of premature infants at greatest risk of developing bronchopulmonary dysplasia and offer therapeutic opportunities via replacement strategies.