TLR Signaling Pathway Gene Polymorphisms, Gene-Gene and Gene-Environment Interactions in Allergic Rhinitis

被引：7
|
作者：
Chen, Ruo-Xi [1 ,2 ]
Dai, Meng-Di [1 ,2 ]
Zhang, Qing-Zhao [1 ,2 ]
Lu, Mei-Ping [1 ,2 ]
Wang, Mei-Lin [3 ,4 ]
Yin, Min [1 ,2 ,5 ]
Zhu, Xin-Jie [1 ,2 ]
Wu, Zhong-Fei [1 ,2 ]
Zhang, Zheng-Dong [3 ,4 ]
Cheng, Lei [1 ,2 ,5 ]
机构：
[1] Nanjing Med Univ, Affiliated Hosp 1, Dept Otorhinolaryngol, 300 Guangzhou Rd, Nanjing 210029, Peoples R China
[2] Nanjing Med Univ, Affiliated Hosp 1, Clin Allergy Ctr, 300 Guangzhou Rd, Nanjing 210029, Peoples R China
[3] Nanjing Med Univ, Collaborat Innovat Ctr Canc Personalized Med, Sch Publ Hlth, Dept Environm Genom,Jiangsu Key Lab Canc Biomarke, 101 Longmian Ave, Nanjing 211166, Peoples R China
[4] Nanjing Med Univ, Ctr Global Hlth, Sch Publ Hlth, Dept Genet Toxicol,Key Lab Modern Toxicol,Minist, Nanjing, Peoples R China
[5] Nanjing Med Univ, Int Ctr Allergy Res, Nanjing, Peoples R China
来源：
JOURNAL OF INFLAMMATION RESEARCH | 2022年 / 15卷
基金：
中国国家自然科学基金;
关键词：
allergic rhinitis; toll-like receptors; CD14; single nucleotide polymorphism; gene-gene interaction; gene-environment interaction; RECEPTOR; 4; POLYMORPHISMS; TOLL-LIKE RECEPTOR-2; PROMOTER POLYMORPHISMS; CD14; GENE; HAY-FEVER; ADULT ASTHMA; IGE LEVELS; ASSOCIATION; ATOPY; CHILDREN;
D O I：
10.2147/JIR.S364877
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Background: Allergic rhinitis (AR) is a nasal inflammatory disease resulting from a complex interplay between genetic and environmental factors. The association between Toll-like receptor (TLR) signaling pathway and environmental factors in AR pathogenesis remains to be explored. This study aims to assess the genetic association of AR with single nucleotide polymorphisms (SNPs) in TLR signaling pathway, and investigate the roles of gene-gene and gene-environment interactions in AR. Methods: A total of 452 AR patients and 495 healthy controls from eastern China were enrolled in this hospital-based case-control study. We evaluated putatively functional genetic polymorphisms in TLR2, TLR4 and CD14 genes for their association with susceptibility to AR and related clinical phenotypes. Interactions between environmental factors (such as traffic pollution, residence, pet keeping) and polymorphisms with AR were examined using logistic regression. Models were stratified by genotype and interaction terms, and tested for the significance of gene-gene and gene-environment interactions. Results: In the single-locus analysis, two SNPs in CD14, rs2563298 (A/C) and rs2569191 (C/T) were associated with a significantly decreased risk of AR. Compared with the GG genotype, the GT and GT/TT genotypes of TLR2 rs7656411 (G/T) were associated with a significantly increased risk of AR. Gene-gene interactions (eg, TLR2 rs7656411, TLR4 rs1927914, and CD14 rs2563298) was associated with AR. Gene-environment interactions (eg, TLR4 or CD14 polymorphisms and certain environmental exposures) were found in AR cases, but they were not significant after Bonferroni correction. Conclusion: The genetic polymorphisms of TLR2 and CD14 and gene-gene interactions in TLR signaling pathway were associated with susceptibility to AR in this Han Chinese population. However, the present results were limited to support the association between gene-environment interactions and AR.
引用
收藏
页码：3613 / 3630
页数：18
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