Interleukin-13 -1112 C/T promoter polymorphism confers risk for COPD: a meta-analysis

PLoS One. 2013 Jul 9;8(7):e68222. doi: 10.1371/journal.pone.0068222. Print 2013.

Abstract

Background: Interleukin (IL)-13, a T-helper type 2 cytokine, plays a critical role in the development of chronic obstructive pulmonary disease (COPD). This meta-analysis was performed to assess the association of IL-13 -1112 C/T promoter polymorphism with COPD susceptibility.

Methods: Published case-control studies from Pubmed and China National Knowledge Infrastructure (CNKI) databases were retrieved. Data were extracted and pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated.

Results: Eight case-control studies in seven articles were included in this meta-analysis. Pooled effect size showed IL-13 -1112 C/T was associated with COPD susceptibility in a codominant genetic model (TT vs CT, OR: 1.82, 95% CI: 1.14-2.92 and TT vs CC, OR: 2.02, 95% CI: 1.10-3.72), indicating individuals with TT genotype had an increased risk for COPD compared with those with CT or CC genotype. According to ethnicity, results indicated IL-13 -1112 C/T was correlated with COPD susceptibility in Arabians (TT vs CT, OR: 2.94, 95% CI: 1.03-8.42 and TT vs CC, OR: 3.05, 95% CI: 1.08-8.59). Moreover, after excluding the study without Hardy-Weinberg equilibrium, the pooled results were robust and no publication bias was found in this study.

Conclusions: This meta-analysis suggests IL-13 -1112 C/T promoter polymorphism is associated with the risk of COPD in Arabians.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Case-Control Studies
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Interleukin-13 / genetics*
  • Odds Ratio
  • Polymorphism, Single Nucleotide*
  • Promoter Regions, Genetic*
  • Publication Bias
  • Pulmonary Disease, Chronic Obstructive / genetics*
  • Risk

Substances

  • Interleukin-13

Grants and funding

This study was supported in part by grants 31000513, 31171103, 81200031 and 81230001 from the National Natural Science Foundation of China. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.