The lung of the preterm fetus is often exposed to antenatal glucocorticoids, and histologic chorioamnionitis is frequent. Clinically and experimentally, antenatal glucocorticoids and/or chorioamnionitis are associated with early lung maturation, but in experimental models, both glucocorticoids and intra-uterine inflammation decrease alveolarization. Experimental chorioamnionitis also can amplify the inflammatory response of the preterm lung to mechanical ventilation. In this article, the hypothesis developed is that bronchopulmonary dysplasia occurs because of repetitive adverse lung exposures, or hits, and that the initial hits may be antenatal glucocorticoid exposure and/or antenatal inflammation.