Gene-gene and gene-environmental interactions of childhood asthma: a multifactor dimension reduction approach

PLoS One. 2012;7(2):e30694. doi: 10.1371/journal.pone.0030694. Epub 2012 Feb 15.

Abstract

Background: The importance of gene-gene and gene-environment interactions on asthma is well documented in literature, but a systematic analysis on the interaction between various genetic and environmental factors is still lacking.

Methodology/principal findings: We conducted a population-based, case-control study comprised of seventh-grade children from 14 Taiwanese communities. A total of 235 asthmatic cases and 1,310 non-asthmatic controls were selected for DNA collection and genotyping. We examined the gene-gene and gene-environment interactions between 17 single-nucleotide polymorphisms in antioxidative, inflammatory and obesity-related genes, and childhood asthma. Environmental exposures and disease status were obtained from parental questionnaires. The model-free and non-parametrical multifactor dimensionality reduction (MDR) method was used for the analysis. A three-way gene-gene interaction was elucidated between the gene coding glutathione S-transferase P (GSTP1), the gene coding interleukin-4 receptor alpha chain (IL4Ra) and the gene coding insulin induced gene 2 (INSIG2) on the risk of lifetime asthma. The testing-balanced accuracy on asthma was 57.83% with a cross-validation consistency of 10 out of 10. The interaction of preterm birth and indoor dampness had the highest training-balanced accuracy at 59.09%. Indoor dampness also interacted with many genes, including IL13, beta-2 adrenergic receptor (ADRB2), signal transducer and activator of transcription 6 (STAT6). We also used likelihood ratio tests for interaction and chi-square tests to validate our results and all tests showed statistical significance.

Conclusions/significance: The results of this study suggest that GSTP1, INSIG2 and IL4Ra may influence the lifetime asthma susceptibility through gene-gene interactions in schoolchildren. Home dampness combined with each one of the genes STAT6, IL13 and ADRB2 could raise the asthma risk.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Asthma / epidemiology
  • Asthma / genetics*
  • Case-Control Studies
  • Child
  • DNA / genetics
  • Female
  • Gene-Environment Interaction*
  • Genetic Predisposition to Disease
  • Genotype
  • Glutathione S-Transferase pi / genetics*
  • Humans
  • Infant, Newborn
  • Interleukin-4 Receptor alpha Subunit / genetics*
  • Intracellular Signaling Peptides and Proteins / genetics*
  • Male
  • Membrane Proteins / genetics*
  • Multifactor Dimensionality Reduction*
  • Polymerase Chain Reaction
  • Polymorphism, Single Nucleotide / genetics*
  • Taiwan / epidemiology

Substances

  • IL4R protein, human
  • INSIG2 protein, human
  • Interleukin-4 Receptor alpha Subunit
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins
  • DNA
  • GSTP1 protein, human
  • Glutathione S-Transferase pi