ABSTRACT
The majority of infants developing bronchopulmonary dysplasia (BPD) in the current era have been delivered at 23 to 28 weeks’ gestation. The pathological hallmarks of BPD in this population are interstitial thickening and an arrest or inhibition of alveologenesis (1). Pulmonary hypertension is a significant adverse outcome in those most severely affected (2). As described elsewhere in this volume, inflammation may play a central role in the development of BPD. Suggested major contributors to inflammation, separately or additively, which leads to BPD are chorioamnionitis (3), hyperoxia (4,5), sepsis (6), and ventilation-induced volutrauma (7). Results from in vitro and in vivo models of lung growth, repair, and injury suggest that immaturity, oxygen concentration, sepsis, and volutrauma may all influence the expression of polypeptide growth factors in the developing lung. Whether the structural changes observed in human BPD reflect an altered pattern of secretion of polypeptide growth factors, the appearance of different factors, or both, is unknown. Available information about the role of polypeptide growth factors during the development of BPD remains sparse. This is in major part due to the limited availability of human tissue from the early stages of disease development and, until relatively recently, uncertainty as to the identity of likely mediators.
