It can be explained by advanced lung maturation in terms of an early elevation of interleukin-1 beta (IL–1β) in lung lavage fluid in the presence of chorioamnionitis, which stimulates the release of corticotrophin-releasing factor and corticotrophin.[78], [79] These hormones enhance the production of cortisol which results in accelerated lung maturation and, therefore, a decrease in the incidence of RDS.[80] Lung maturation is also explained with animal models of fetal inflammation. This evidence concerns the gene IL1B and newborn respiratory distress syndrome.