Lack of association between IRAK2 genetic variants and aspirin exacerbated respiratory disease

被引:0
|
作者
Kim, Jason Yongha [1 ]
Kim, Jeong-Hyun [1 ]
Park, Byung-Lae [2 ]
Cheong, Hyun Sub [2 ]
Bae, Joon Seol [1 ]
Park, Jong Sook [3 ]
Kim, Yong-Hoon [4 ]
Kim, Mi-Kyeong [5 ]
Choi, Inseon S. [6 ]
Cho, Sang Heon [7 ,8 ]
Choi, Byoung Whui [9 ]
Park, Choon-Sik [3 ]
Shin, Hyoung Doo [1 ,2 ]
机构
[1] Sogang Univ, Dept Life Sci, Seoul 121742, South Korea
[2] SNP Genet Inc, Dept Genet Epidemiol, Seoul, South Korea
[3] Soonchunhyang Univ, Seoul Hosp, Div Allergy & Resp Med, Seoul 140743, South Korea
[4] Soonchunhyang Univ, Cheonan Hosp, Div Allergy & Resp Dis, Cheonan, South Korea
[5] Chungbuk Natl Univ, Div Internal Med, Cheongju, South Korea
[6] Chonnam Natl Univ, Dept Allergy, Kwangju, South Korea
[7] Seoul Natl Univ, Dept Internal Med, Seoul, South Korea
[8] Seoul Natl Univ, Inst Allergy & Clin Immunol, Seoul, South Korea
[9] Chung Ang Univ, Dept Internal Med, Yongsan Hosp, Seoul 156756, South Korea
关键词
Aspirin exacerbated respiratory disease; Haplotype; IRAK2; Single nucleotide polymorphism; INTOLERANT ASTHMA; POLYMORPHISMS; DIAGNOSIS;
D O I
10.1007/s13258-013-0058-8
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Asthma is a global health problem which threatens approximately 300 million patients worldwide. Among them, up to 20 % of the asthma patients are classified as aspirin exacerbated respiratory disease (AERD). Interleukin-1 receptor associated kinase (IRAK2) is associated with necrosis factor kappa B (NF-(DB)-B-0) pathway via interleukin-1 (IL-1) signaling. NF-(DB)-B-0 pathway is known to be involved in asthma development, and several interleukin and IRAK family members have also been reported to be associated with asthma or AERD. Since IRAK2 plays an important role in the asthma etiology, we hypothesized that the genetic variants of IRAK2 may be associated with AERD. This study genotyped a total of 25 common single nucleotide polymorphisms (SNPs) in 163 AERD cases and 429 aspirin-tolerant asthma (ATA) controls. As a result, no significant association was found between the genetic variants of IRAK2 and AERD (P > 0.05). In further regression analysis for the forced expiratory volume in 1 s (FEV1) decline, an important phenotype for diagnosing AERD, although one haplotype (BL1_ht3) showed a nominal association with FEV1 decline (P = 0.04), the significance disappeared after correction for multiple testing (P > 0.05). Despite limitations in our study and need for replications, our results suggest that the genetic variants of IRAK2 might not be associated with AERD and the obstructive symptoms in asthma.
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收藏
页码:475 / 482
页数:8
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