Nonassociation of interleukin 4 intron 3 and 590 promoter polymorphisms with bronchopulmonary dysplasia for ventilated preterm infants

Interleukin 4 (IL-4) stimulates and amplifies the inflammatory response, stimulates collagen synthesis in fibroblasts, promotes the progression to fibrosis and has been shown to inhibit the production of several inflammatory cytokines in the development of bronchopulmonary dysplasia (BPD) and airway hyperreactivity. We aimed to investigate whether IL-4 polymorphisms in ventilated preterm infants were associated with BPD. BPD was defined as infants who remained dependent on active respiratory support or oxygen supplementation at 36 weeks postconceptional age. A case-control study of 224 preterm infants (<30 weeks) who had respiratory distress syndrome and needed intermittent mandatory ventilation (IMV) were undertaken between January 1999 and December 2003. The typing of each genetic polymorphism was performed by polymerase-chain-reaction-based restriction analysis. Genotype distribution and allelic frequencies were compared between ventilated preterm infants who developed BPD and those who did not and the duration of IMV. The demography of these ventilated BPD and non-BPD preterm infants was not different. We observed no significant differences in genotype distribution or allelic frequency of the IL-4 intron 3 or IL-4 promoter polymorphisms between ventilated preterm infants who developed BPD and who did not. There was no significant association of the genotype or allelic frequency of IL-4 polymorphism with duration of IMV. We conclude that neither IL-4 intron 3 nor the 590 promoter polymorphism is a useful marker for predicting the susceptibility to BPD in ventilated Taiwanese preterm infants.