The A/A genotype of an interleukin-17A polymorphism predisposes to increased severity of atopic dermatitis and coexistence with asthma

Abstract

Studies have found that the interleukin-23/T helper 17 (IL-23/Th17) pathway plays an important role in the pathogenesis of atopic dermatitis (AD). Inhibition of the IL-23/Th17 pathway with monoclonal antibodies reduces skin inflammation in animal models. To investigate the association between IL-17A and IL-23R gene single nucleotide polymorphisms (SNPs) and the development of AD in a Polish population. Blood samples were collected from 166 patients with AD and 160 controls. We analyzed two SNPs, -152 G/A IL-17A and 1142 G/A IL-23R, using PCR and restriction fragment length polymorphism (RFLP) analysis. There was no statistically significant difference between the examined IL-17A SNP and the incidence of AD (P>0.05 for all comparisons). Analysis of the IL-23R gene SNP showed no relationship between AD and the G/A genotype or presence of the A allele. The study did not establish any links between the IL-23R and IL-17A gene SNPs and the likelihood of developing AD resulting from gene-gene interaction. However, there was a significant relationship between the A/A genotype in the -152 G/A IL1-7A SNP and the coexistence of AD and asthma (P<0.04). Analyzing the association between AD severity and the occurrence of IL-17A SNP, we found that subjects with the A/A genotype were at higher risk of developing moderate or severe AD (P=0.02). We found no evidence of any effect of IL-17A or IL-23R SNPs on the occurrence of AD in our Polish population. However, the A/A genotype in IL-17A was found to predispose to increased AD severity and coexistence of AD and asthma.