Identification of polymorphisms in the Toll-like receptor gene and the association with allergic rhinitis

摘要

The TLRs gene encodes the principal innate immunity receptor in humans. The TLR2 Arg753Gln and Arg677Trp polymorphisms have been associated with a reduced response of monocytes and cell lines to challenge with mycobacteria. The TLR4 Asp299Gly and Thr399Ile polymorphisms have been associated with a reduction in the inflammatory responses to lipopolysaccharide in humans. It has been suggested that TLR2 and TLR4 polymorphisms may be associated with allergic responses; thus, we hypothesized that TLR2 and TLR4 polymorphisms may modify the relative risk for development of allergic rhinitis. The Taqman assay and high-resolution melt (HRM) were used for genotyping. We analyzed two single nucleotide polymorphisms (SNPs; 597T>C and 1350T>C) in the TLR2 gene and 1 SNP (4216G>C) in the TLR4 gene. We compared the genotype of these SNPs in patients with allergic rhinitis and controls without allergic rhinitis. We also estimated the haplotype frequencies between the two groups. The genotype and allele frequencies of the 597T>C and 1350T>C SNPs in the TLR2 gene were not significantly different between the patients with allergic rhinitis and controls (P > 0.05). The genotype and allele frequencies of 4216G>C in the TLR4 gene were not significantly different between the patients with allergic rhinitis and controls (P > 0.05). Haplotype analysis of the following two different (597)–(1350) major haplotypes (frequency >0.05) were present in the TLR2 gene: T–C and C–C. The C–C haplotype was positively associated with allergic rhinitis (P = 0.048). Our study suggests that the TLR2 gene polymorphisms might be susceptible to the development of allergic rhinitis. Further functional studies of TLR2 genetics in light of the associations with allergic rhinitis inflammation would help clarify the role of TLR2 genetics in clinical evaluations. Keywords Toll-like receptor - Innate immunity - Allergic rhinitis - Polymorphism I. Kang and Y.-K. Oh contributed equally to this paper.