Association of asthma with a functional promoter polymorphism in the IL16 gene

J Allergy Clin Immunol. 2006 Jan;117(1):86-91. doi: 10.1016/j.jaci.2005.10.011.

Abstract

Background: IL-16, a multifunctional cytokine with increased expression in the airways of asthmatic subjects, inhibits allergic airway inflammation in animal models. A T-->C single nucleotide polymorphism (SNP) at the -295 position in the promoter region of the IL16 gene has been described.

Objective: We sought to examine the functional significance of this promoter SNP and its relationship to asthma.

Methods: We examined the effect of the -295 SNP on promoter activity in cell-line (HBE4-E6/E7) transfection experiments. We investigated the association of the IL16 -295 genotype with asthma among 341 affected sib-pair white families and 184 unrelated nonasthmatic control subjects. We analyzed the association between the IL16 genotype and asthma using family-based association test and case-control analyses.

Results: In in vitro transfection experiments the T allele in the -295 position was associated with substantially reduced promoter activity compared with the C allele. In the family study the more common T allele at the -295 position was significantly associated with all asthma phenotypes (P = .002 to P = .015). In the case-control analysis asthmatic subjects were more likely than unrelated nonasthmatic control subjects to have the -295 TT genotype, but this did not reach statistical significance (odds ratio, 1.36; 95% CI, 0.92-2.02).

Conclusions: The T allele at the -295 position in the IL16 promoter region is associated with reduced promoter activity relative to the C allele and with asthma in this white population. Further investigation is needed to delineate the mechanisms underlying these findings and the relationship of the IL16 -295 genotype to asthma in other populations.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Asthma / genetics*
  • Case-Control Studies
  • Child
  • Female
  • Humans
  • Interleukin-16 / genetics*
  • Male
  • Odds Ratio
  • Polymorphism, Single Nucleotide*
  • Promoter Regions, Genetic*
  • Transfection

Substances

  • Interleukin-16