The association between toll-like receptor 2 expression and gene polymorphism with seborrheic dermatitis patients

Introduction: Seborrheic dermatitis (SD) is a common chronic inflammatory skin condition, characterized by scaling and poorly defined erythematous patches. The etiopathogenesis of SD remains unknown, although many factors have been implicated. Malessezia furfur has been implicated in the development of this condition. The family of Toll-like receptors (TLRs) is a key role in host immunity by mediating inflammatory reactions against a wide range pathogens. Polymorphism in TLRs have revealed the importance of TLRs in human defence against diseases. The TLR2 expression and gene polymorphism linked with impaired reactivity to Malessezia furfur may play role in pathogenesis of seborrheic dermatitis. Aim: The aim of the present study was to investigate the Toll-like receptor 2 (TLR2) gene polymorphism and TLR2 expression in seborrheic dermatitis patient compared to healthy controls. Materials and Methods: Genomic DNA was obtained from the peripheral blood of 60 patients with SD and 60 healthy subjects. The TLR2 Arg753Gln gene polymorphism were genotyped by the polymerase chain reaction- restriction fragment length polymorphism method. Surface expression of TLR2 on the monocytes was also assessed by means flow cytometry. The data were analysed by a x2 test, logistic regression analysis and the Hardy-Weinberg equilibrium test. Results: The Arg753Gln mutant genotype was found in 20% of the seborrheic dermatitis patients. Arg753Gln single nucleotide polimorfism was not seen in the control group. The frequency of the A allele was 9,8% in seborrheic dermatitis patients. For the healthy subjects, A allele was not detected (p<0,0001). Compared with healthy controls, the TLR2 Arg753Gln genotype was significantly higher in the entire group of seborrheic dermatitis cases (p<0.0001). While TLR2 expression on monocytes mean rate was 72,9±3,1% in the patients group, this rate was 80,7±2,7% in healty group. However, there was no significant difference in TLR2 expression rates (p=0,129). At the same time, compared with non-mutant SD patients, the TLR2 expression on monocytes was significantly lower in patients with TLR2 Arg753Gln mutant SD patients (p=0,03). Conclusion: We show for the first time TLR2 R753Q single nucleotide polymorphism in SD patients. We also determined that TLR2 R753Q mutation is associated with lower expressions of TLR2 on monocytes. TLR2 may be essential in the pathogenesis and maintenance of SD and may be involved in the enhanced susceptibility to skin colonization with M. furfur in patient with SD carrying TLR2 polymorphism.