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

• Published in: Clinical and experimental dermatology Vol. 40; no. 1; pp. 11 - 16
• Main Authors: Narbutt, J., Wojtczak, M., Zalińska, A., Salinski, A., Przybylowska-Sygut, K., Kuna, P., Majak, P., Sysa-Jedrzejowska, A., Lesiak, A.
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.01.2015; Oxford University Press
• Subjects: Adolescent; Adult; Alleles; Asthma - complications; Case-Control Studies; Child; Child, Preschool; Dermatitis, Atopic - complications; Dermatitis, Atopic - epidemiology; Dermatitis, Atopic - genetics; Female; Gene Frequency; Genetic Predisposition to Disease; Genotype; Humans; Incidence; Infant; Interleukin-17 - genetics; Male; Poland - epidemiology; Polymorphism, Restriction Fragment Length; Polymorphism, Single Nucleotide; Receptors, Interleukin - genetics; Severity of Illness Index; Young Adult; Poland
• ISSN: 0307-6938; 1365-2230; 1365-2230
• DOI: 10.1111/ced.12438

Summary Introduction 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. Aim To investigate the association between IL‐17A and IL‐23R gene single nucleotide polymorphisms (SNPs) and the development of AD in a Polish population. Methods 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. Results 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). Conclusions 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.