Get access
Clinical & Experimental Allergy

Interleukin-10 gene promoter region polymorphism is associated with eosinophil count and circulating Immunoglobulin E in adult asthma

Authors


Jussi Karjalainen, University of Tampere Medical School, FIN-33014 University of Tampere, Finland. E-mail: jussi.karjalainen@ uta.fi

Summary

Background IL-10 has several functional effects relevant to asthma. It can modulate IgE production and induce apoptosis in eosinophils. Polymorphisms of IL-10 gene have been shown to affect IL-10 production.

Objective To establish whether IL-10 polymorphisms are associated with asthma and phenotype-related characteristics.

Methods The frequency of three single base exchange polymorphisms (at positions − 1082, − 819 and − 592) and corresponding haplotypes of the IL-10 gene were analysed in 245 adult asthmatic subjects and 405 controls using PCR and restriction fragment length polymorphism (RFLP). The data were assessed for correlations with the eosinophil count, serum IgE and lung function.

Results The IL-10 haplotype frequencies were similar in asthmatics and controls. Eosinophil count median was 2.0- to 3.2-fold higher among asthmatics with rare ATA/ATA genotype than in asthmatics with other genotypes. No such difference was seen in the control group. When analysed by IL-10 haplotype carrier state and gender, male asthmatics with ATA haplotype had 2.8-fold higher serum IgE than those without ATA. A converse association was found in male controls with ATA haplotype, who had 1.9-fold lower serum IgE than their ATA-negative counterparts. The high IL-10-producing GCC haplotype was associated with impaired lung function in smoking male controls while in asthmatics no clear effect on lung function was found with any of the haplotypes studied.

Conclusion These results suggest that the eosinophil counts and serum IgE are differently regulated by IL-10 genotype in asthmatic and in normal subjects. However, IL-10 polymorphism is not related to susceptibility in asthma.

Get access to the full text of this article

Ancillary