Single nucleotide polymorphisms of tumor necrosis factor-alpha and the susceptibility to bronchopulmonary dysplasia.

Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease of infancy. A "New" BPD has been characterized in preterm infants that may begin in utero, and then progress post-natally, resulting in arrested lung development and alveolar hypoplasia. Foundations for this "New" BPD may be derived from pro-inflammatory genes including tumor necrosis factor-alpha (TNFalpha). The hypothesis of the current study is that single nucleotide polymorphisms (SNPs) of the pro-inflammatory TNFalpha gene place preterm infants at increased risk for BPD. Preterm infants (105 in number) with birthweights

The genetic basis for bronchopulmonary dysplasia.

While the 'original' bronchopulmonary dysplasia (BPD) was attributed to the iatrogenic effects of oxygen and barotrauma on the preterm lung, analyses of the 'new' BPD suggests that these environmental effects may contribute to arrested pulmonary development, and that there may also be genetic foundations for the susceptibility to BPD. Twinning, family and population studies implicate heritable factors in the evolution of BPD. The candidate genes examined for their potential role in BPD include surfactant apoprotein and inflammatory genes. With the identification and mapping of single nucleotide polymorphisms (SNPs), an explosion of testing for these genetic components that may contribute to a number of complex, multigenic disease conditions-including BPD-have been initiated. Sophisticated multiplex analyses are now available to link candidate SNPs to conditions such as BPD. However, there continues to be wide variation in the expression of BPD throughout neonatal units. Differentiating the effects caused by environmental and environmental-genetic interactions from isolated genetic etiologies is still problematic and will require carefully designed genetic analyses of preterm infant groups and their families.