Although immaturity, barotrauma, and oxygen toxicity contribute to the pathogenesis of bronchopulmonary dysplasia (BPD), the exact mechanisms by which the neonatal lung undergoes such severe disruption in structure and function is not fully understood. The potential role of inflammation and infection in the process of BPD is suggested by several cytological, histopathological, and clinical studies.

Within minutes, oxygen exposure and positive pressure ventilation can produce epithelial and endothelial cell injury leading to the leak of protein-rich fluid from the pulmonary microcirculation into the interstitium, with resultant edema and respiratory failure. 10311 Compared to adults the lungs of very premature neonates are more susceptible to damage because of immaturity of pulmonary cell junctions, I2 low levels of protective antioxidant enzymes, I3 low levels of surfactant, I4 and low concentrations of factors promoting lung differentiation and regeneration. l5 After lung injury, a reparative process occurs involving many blood elements including platelets, neutrophils, and alveolar macrophages. Preterm neonates at risk for the development of BPD have shown an enhanced inflammatory reaction in the lungs with an associated increase in pulmonary microvascular permeability. I6 One of the functions of these cells during the early phase of inflammation is removal of debris from injured tissue. However, they also contribute to the destructive process by releasing proteolytic enzymes3 and toxic oxygen metabolites" which damage pulmonary cells and alter their function.