It can result from intrauterine infections or inflammatory conditions such as chorioamnionitis, and the consequences for the newborn can include respiratory, neurological, and other health complications [11,12]. However, studies show that intrauterine inflammation (histological chorioamnionitis or funisitis) may reduce the risk of RDS by accelerating fetal lung maturation via enhanced surfactant synthesis. Pro-inflammatory cytokines in intrauterine inflammation (e.g., interleukin-6, prostaglandin E2) stimulate surfactant production, improving lung function [13-15]. This evidence concerns the gene IL6 and chorioamnionitis.