Article Text

  1. G Prencipe1,
  2. F DeBenedetti1,
  3. R Inglese2,
  4. M P Ronchetti3,
  5. R Devito4,
  6. C Corchia3,
  7. G Seganti3,
  8. A E Tozzi5,
  9. M Orzalesi3,
  10. C Auriti3
  1. 1Rheumatology Research Laboratory, Bambino Gesù Children’s Hospital, Rome, Italy,
  2. 2Clinical Chemistry Laboratory, Bambino Gesù Children’s Hospital, Rome, Italy,
  3. 3Department of Neonatology, Bambino Gesù Children’s Hospital, Rome, Italy,
  4. 4Division of Pathology, Bambino Gesù Children’s Hospital, Rome, Italy,
  5. 5Epidemiology Unit, Bambino Gesù Children’s Hospital, Rome, Italy


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.

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.