Pulmonary inflammation is a key feature in the pathogenesis of bronchopulmonary dysplasia (BPD). This inflammatory process, induced by multiple risk factors, is characterized by the presence of inflammatory cells, cytokines and an arsenal of additional humoral mediators in the airways and pulmonary tissue of preterm infants with the condition. Several mediators have a direct detrimental effect on pulmonary structures by affecting cell integrity and inducing apoptosis. An imbalance between pro-inflammatory and anti-inflammatory factors can generally be considered to be a hallmark of lung injury. Intrauterine exposure to pro-inflammatory cytokines or antenatal infection may prime the fetal lung such that minimally injurious postnatal events provoke an excessive pulmonary inflammatory response that most certainly affects normal alveolization and pulmonary vascular development in preterm infants with BPD.