ABSTRACT
Bronchopulmonary dysplasia (BPD) is an evolving process of lung injury that can result in chronic impairment of lung function and may have lifelong consequences for the infant. Pre-and postnatal factors have been shown to induce an injurious inflammatory response in the immature airways and the pulmonary interstitium of preterm infants, which may subsequently affect normal alveolarization and pulmonary vascular development. More than half of very immature infants may have been exposed to chorioamnionitis, and a considerable number of them are born with inflamed lungs and signs of fetal inflammatory response. In addition, various postnatal factors such as resuscitation, high airway concentrations of inspired oxygen, mechanical ventilation, and pulmonary as well as systemic infections may perpetuate or even amplify an injurious inflammatory response in the airways and interstitium. The etiology of BPD is definitely multifactoral, and the multiple-hit theory offers a plausible concept that can help to explain the complex pathogenetic mechanisms involved in this chronic lung disease of very immature preterm infants (1,2). This actualized chapter summarizes, in a condensed form, the current pathogenetic concepts on the possible role of inflammation in the evolution of BPD and expands on previously published review articles (3-6).
