ArticleCentral-European journal of immunology2017
The significance of IL-1β +3953C>T, IL-6 -174G>C and -596G>A, TNF-α -308G>A gene polymorphisms and 86 bp variable number tandem repeat polymorphism of IL-1RN in bronchopulmonary dysplasia in infants born before 32 weeks of gestation.
Article in Central-European journal of immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Association of TNF-α genetic variants with neonatal bronchopulmonary dysplasia: consolidated results.Frontiers in pediatrics · 2024Pooled it
- Analysis of the Role of Gene Variants in Matrix Metalloproteinases and Their Tissue Inhibitors in Bronchopulmonary Dysplasia (BPD): A Study in the Polish Population.Current issues in molecular biology · 2025Article
- Genetic and Epidemiological Similarities, and Differences Between Postoperative Intraperitoneal Adhesion Development and Other Benign Fibro-proliferative Disorders.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- The Change of Cytokines and Gut Microbiome in Preterm Infants for Bronchopulmonary Dysplasia.Frontiers in microbiology · 2022Article
- Cytokines and Exhaled Nitric Oxide Are Risk Factors in Preterm Infants for Bronchopulmonary Dysplasia.BioMed research international · 2021Article
- Association of Variants in IL6-Related Genes with Lung Cancer Risk in Moroccan Population.Lung · 2019Article
- Vitamin D and IL-10 Deficiency in Preterm Neonates With Bronchopulmonary Dysplasia.Frontiers in pediatrics · 2018Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionBronchopulmonary dysplasia (BPD) is a chronic lung disease that affects primarily preterm infants. Genetic factors are also taken into consideration in the pathogenesis of BPD. Genetic predispositions to higher production of inflammation mediators seem to be crucial. MATERIAL AND
methodsThe aim of this study was to evaluate the possible relationship between polymorphisms: interleukin-1β +3953 C>T, interleukin-6 -174 G>C and -596 G>A, tumour necrosis factor -308 G>A and interleukin-1RN VNTR 86bp and the occurrence of BPD in a population of 100 preterm infants born from singleton pregnancy, before 32+0 weeks of gestation, exposed to antenatal steroids therapy, and without congenital abnormalities.
resultsIn the study population BPD was diagnosed in 36 (36%) newborns. Among the studied polymorphisms we found the higher prevalence for BPD developing of the following genotypes: 1/2 (OR 1.842 [0.673-5.025] and 2/2 IL-1RN (OR 1.75 [0.418-6.908] 86bpVNTR; GC (2.222 [0.658-8.706]) and CC IL-6 -174G>C (1.6 [0.315-8.314]) and GA (2.753 [0.828-10.64]) and AA (1.5 [0.275-8.067] IL-6 -596G>A), GA 1.509 (0.515-4.301) TNF-α -308G>A. However, these finding were not statistically significant.
conclusionsGenetic factors are undeniably involved in the pathogenesis of BPD. In the times of individualised therapy finding genes responsible for BPD might allow the development of new treatment strategies. A new way of specific therapy could ensure the reduction of complications connected with BPD and treatment costs.
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