There is a strong evidence that histologic chorioamnionitis is associated with a reduction of incidence and severity of respiratory distress syndrome (RDS). Short-term maturational effects on the lungs of extremely premature infants seem to be, however, accompanied by a greater susceptibility of the lung, eventually contributing to an increased risk of bronchopulmonary dysplasia (BPD). Genetic susceptibility to BPD is an evolving area of research and several studies have directly related the risk of BPD to genomic variants. There is a substantial heterogeneity across the studies in the magnitude of the association between chorioamnionitis and BPD, and whether or not the association is statistically significant. Considerable variation is largely dependent on differences of inclusion and exclusion criteria, as well as on clinical and histopathological definitions. The presence of significant publication bias may exaggerate the magnitude of the association. Controlling for publication bias may conduct to adjusted results that are no longer significant. Recent studies generally seem to confirm the effect of chorioamnionitis on RDS incidence, while no effect on BPD is seen. Recent data suggest susceptibility for subsequent asthma to be increased on long-term followup. Additional research on this field is needed. 1. Introduction Watterberg and colleagues [1] were the first to report, in 1996, a decrease in the incidence of respiratory distress syndrome (RDS), while the incidence of chronic lung injury, marked by the presence of bronchopulmonary dysplasia (BPD), was increased in preterm newborns with histological chorioamnionitis. This paradoxical effect of prenatal inflammation on pulmonary outcome has been referred to as the “Watterberg effect.” Since then, the effects of antenatal inflammation on both short- and long-term pulmonary outcome have received increasing attention, and many studies have been reported over the last years. Chorioamnionitis is the leading cause of very preterm delivery and its incidence increases with decreasing gestational age [2–5]. BPD is one of the most frequent sequelae in very preterm infants and results in increased healthcare costs, prolonged hospital stays with frequent readmissions, and deleterious effects on subsequent growth and neurodevelopment [6, 7]. BPD is mostly multifactorial and a complex view of its pathogenesis (“multiple hits” hypothesis) has emerged, which includes antenatal exposure to a proinflammatory environment together with various postnatal inflammation-triggering events such as mechanical ventilation,
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