Background: In preterm neonates bronchopulmonary dysplasia (BPD) is a common disease causing severe morbidity and mortality. Although prematurity, barotrauma and pulmonary oxygen toxicity are well-known risk factors in the pathogenesis of BPD, current evidence suggests an interindividual variability and susceptibility. MIF is a regulator of the innate immune response that has recently been implicated in murine fetal lung development and in surfactant production by pulmonary epithelium and plays a possible role in lung development in humans (Kevill KA. J Immunol 2008). The human MIF promoter gene contains a functionally relevant –173G/C polymorphism, with the G allele associated with low gene expression and low MIF serum levels.
Aims: To investigate the relationship between MIF genotype and the occurrence of BPD.
Methods: We determined the MIF-173G/C genotype in a prospective cohort of 89 preterm neonates (gestational age ⩽34 weeks) with respiratory distress syndrome, observed from neonatal intensive care unit admission to discharge.
Results: 22/89 neonates (24.7%) developed BPD, defined as oxygen requirement at 36 weeks post-conceptional age. The frequency of neonates with the G/G genotype who developed BPD (37.0%) was higher (p = 0.03) than that of neonates carrying the C allele (9.1%). After adjusting for birth weight, days of mechanical ventilation and of O2 therapy, the G/G genotype remained associated with BPD (p = 0.018, odds ratio 254.5, 95% CI 2.5 to >1000).
Conclusions: Our results, in humans, identify the low MIF producer G/G promoter genotype as a risk factor for BDP and support a role of MIF in lung maturation.
This study was approved by the hospital ethics committee.
Funding: Supported by a grant from the Italian Ministry of Health.
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