Single Nucleotide Polymorphism of Dectin-1 Gene Associates with Atopic Dermatitis in Children

Abstract

BACKGROUND: Atopic dermatitis (AD) is a chronic inflammatory skin disease with complex and multifactorial pathophysiology, involving elements of barrier dysfunction, alterations in cell-mediated immune responses, IgE sensitization, and environmental factors. This encourages the search for predictors of disease development among both genetic markers and environment. AIM: The aim of the study was to examine if genetic factors of Malassezia recognition, or Malassezia colonization may be related to IgE sensitization or to severity of AD. METHODS: The study included 106 patients with eczema and 103 healthy children. Specific IgE against Malassezia mix (m227) was analyzed in 51 patients using immunochemiluminescent method on the ImmunoCAP 100 (Thermo Fisher Scientific Inc., Phadia, Sweden). Genotyping for rs7309123 in Dectin-1 was performed using Real-time PCR. The level of colonization by Malassezia in the scale samples was determined by a real-time PCR assay. RESULTS: Increased IgE to Malassezia spp. was observed in 29,4% of children with eczema. Higher Malassezia spp. – specific IgE titer positively correlated with severity of AD, age of onset, head–neck type of AD, and a higher total IgE. GG genotype rs7309123 Dectin-1 is significantly more often found in the patients than in the control group, but no correlation with IgE sensitization to Malassezia was found. Malassezia restricta and M. globosa were predominant in patients and controls, with some predominance of M. globosa over M. restricta among patients. CONCLUSION: Sensitization to Malassezia, genetic markers in Dectin-1, and Malassezia colonization of the skin can be tools for studying the gene-environment interactions in the pathogenesis of AD.