中国汉族人群Clara细胞10-kDa蛋白基因变异与慢性鼻窦炎缺乏相关性

Feng Zhang, Zhi-Gang Xiong, Ping-Ping Cao, Xue-Jun You, Qi-Xue Gao, Yong-Hua Cui, Zheng Liu
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引用次数: 6

摘要

背景:Clara细胞10-kDa蛋白(CC10)是一种抗炎分子,参与哮喘和慢性鼻窦炎(CRS)的发病机制。CC10基因(A + 38G)的单核苷酸多态性(SNP)先前被证明与哮喘和血浆CC10水平相关。本研究的目的是研究中国中部汉族人群中CC10 A + 38G SNP、血浆CC10水平和CRS之间是否存在关联。方法:采用限制性片段长度多态性聚合酶链反应分析220例CRS患者(伴有鼻息肉90例,无鼻息肉130例)和180例健康对照者血浆CC10水平,采用酶联免疫吸附法检测CC10 A + 38G SNP。220例CRS患者中,108例为特应性受试者。CRS患者的疾病严重程度通过冠状位计算机断层扫描(CT)确定,并根据Lund和Mackay分级。结果:A等位基因的频率为0.394,除德国人外,与其他报告民族的频率均不显著升高。CC10 A + 38G SNP与CRS、CRS亚组或CRS严重程度均无相关性。尽管在CRS和对照组中,AA基因型受试者的血浆CC10浓度显著低于GG和GA基因型受试者(p = 0.00),但血浆CC10水平与CRS表型之间没有相关性。结论:CC10 A + 38G SNP可能对中国汉族人群CRS的发展没有实质性影响。
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Lack of association of Clara cell 10-kDa protein gene variant with chronic rhinosinusitis in a Chinese Han population.

Background: Clara cell 10-kDa protein (CC10) is an anti-inflammatory molecule and has been implicated in the involvement of the pathogenesis of asthma and chronic rhinosinusitis (CRS). A single nucleotide polymorphism (SNP) in CC10 gene (A + 38G) was previously shown to be associated with asthma and plasma CC10 levels. The purpose of this study is to examine whether there is an association between the CC10 A + 38G SNP, plasma CC10 levels, and CRS in a central Chinese population of Han nationality.

Methods: The CC10 A + 38G SNP was analyzed by means of polymerase chain reaction with restriction fragment length polymorphism and plasma CC10 levels were measured using enzyme-linked immunosorbent assay in 220 patients with CRS (90 patients with nasal polyps [NPs] and 130 patients without NPs) and 180 healthy control subjects. Among 220 patients with CRS, 108 patients were atopic subjects. Severity of disease was determined by coronal computed tomography (CT) scan in CRS patients, which was graded according to Lund and Mackay.

Results: The frequency of the A allele was 0.394, which was not significantly higher than the frequencies of other reported ethnic groups except for German. No association between the CC10 A + 38G SNP and CRS, any subgroup of CRS, or CRS severity could be found. Although subjects carrying the AA genotype had a significantly lower plasma CC10 concentration than those carrying the GG and GA genotypes in both CRS and control groups (p = 0.00 for all), no association was found between the plasma CC10 levels and CRS phenotype.

Conclusion: The CC10 A + 38G SNP may not exert a substantial influence on the development of CRS in the Chinese Han population.

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