Objective: The aim: Malassezia has been linked to atopic dermatitis, and TLRs are suggested to mediate influence of Malassezia spp on human cells. The aim of the study was to examine if TLR2 rs4696480 polymorphism predisposes to atopic dermatitis, IgE sensitization to Malassezia or to severe phenotype of atopic dermatitis.
Patients and methods: Materials and methods: The study included 103 patients with eczema and 84 healthy children. Specific IgE against Malassezia mix (m227) was analyzed in 47 patients using immunochemiluminescent method on the ImmunoCAP 100 (Thermo Fisher Scientific Inc., Phadia, Sweden). Genotyping for TLR2 rs4696480 was performed by using Real-time PCR.
Results: Results: Increased IgE to Malassezia spp. was observed in 34,3 % of children with eczema. Higher Malassezia spp.-specific IgE titre positively correlated with duration of atopic dermatitis and a higher total IgE. There were no difference in allele distribution among patients and control group (OR=1.096 (0.549- 2.191) for AT, OR=0.946 (0.430- 2.078) for TT, р > 0,05). TLR2 polymorphism rs4696480 was not associated with Malassezia spp.-sIgE. AA-genotype was significantly more frequent among patients with severe and moderate-to-severe AD (OR=6.395 (1.240-32.991).
Conclusion: Conclusions: AA variant of TLR2 rs4696480 polymorphism predisposes to severe phenotype of AD.
Keywords: Malassezia; SNP; TLR2; atopic dermatitis; children.