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Published on: May 10, 2024
Single nucleotide polymorphisms of tumor necrosis factor-alpha and the susceptibility to bronchopulmonary dysplasia
Sonya S Strassberg1, Ioana A Cristea, Dajun Qian
1Department of Pediatrics, Division of Neonatology, New York Medical College, Maria Fareri Children's Hospital of Westchester Medical Center, Valhalla, NY 10595, USA. strassbergs@wcmc.com
Insights
This study investigated if tumor necrosis factor-alpha (TNFalpha) gene variations increase the risk of bronchopulmonary dysplasia (BPD) in preterm infants. No significant association was found between TNFalpha single nucleotide polymorphisms (SNPs) and BPD severity.
Area of Science:
- Neonatology
- Genetics
- Pulmonology
Background:
- Bronchopulmonary dysplasia (BPD) is a common chronic lung disease in infants.
- A "New" BPD phenotype involves arrested lung development, potentially influenced by pro-inflammatory genes like tumor necrosis factor-alpha (TNFalpha).
Purpose of the Study:
- To determine if single nucleotide polymorphisms (SNPs) in the TNFalpha gene are associated with an increased risk or severity of BPD in preterm infants.
Main Methods:
- Analyzed DNA from 105 preterm infants (<1 kg birthweight) for five TNFalpha SNPs (-1,031, -863, -857, -308, -238).
- Reconstructed haplotypes and estimated frequencies using PHASE software.
- Stratified infants for BPD severity based on oxygen requirements.
Main Results:
- No significant association was found between BPD severity and common 5-marker TNFalpha haplotypes.
- No significant association was observed for three-SNP haplotypes (-1,031, -863, -857) or two-SNP haplotypes (-308, -238).
- The five investigated TNFalpha SNPs showed no association with BPD severity.
Conclusions:
- The study found no evidence that the investigated TNFalpha gene SNPs or their haplotypes are associated with the severity of bronchopulmonary dysplasia in preterm infants.
Abstract:
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
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Single Nucleotide Polymorphisms-SNPs
