Candelaria Pierre V, Backer Vibeke, Laing Ingrid A, Porsbjerg Celeste, Nepper-Christensen Steen, de Klerk Nick, Goldblatt Jack, Le Souëf Peter N
School of Paediatrics and Child Health, University of Western Australia, GPO Box D184, Perth, Western Australia, Australia, 6840.
Immunogenetics. 2005 Apr;57(1-2):25-32. doi: 10.1007/s00251-005-0778-2. Epub 2005 Mar 3.
The gene for Clara cell 16-kDa (CC16) protein is a promising candidate for asthma susceptibility. The CC16 38A allele has been associated with decreased CC16 plasma levels and increased incidence of asthma in Australian children. To date these results have not been replicated in adults. Therefore, potential links between CC16 A38G, asthma and atopy were investigated in an unselected population of young adult Danes. Four hundred sixty-four Danes, aged 19-29 years, from Copenhagen participated in an asthma and allergy phenotype-genotype study. Genotyping was done by Sau96I restriction digestion of PCR products spanning the A38G polymorphism. Potential A38G genotype and asthma-related phenotype associations were investigated using regression analysis, adjusting for potential confounders where appropriate. Adults with the 38AA genotype had higher odds of current asthma (OR 3.2, P=0.013) and ever asthma (OR 2.2, P=0.045) compared with those with the 38GG genotype. Adjusting for atopy had minimal effect on this relationship. A positive linear trend was evident between the 38A allele and atopic dermatitis (OR 1.67, P=0.02). No associations were found between the A38G polymorphism and rhinitis, atopy, forced expiratory volume in 1 s (FEV(1)), forced vital capacity (FVC), airway responsiveness (AR) to histamine or peripheral blood eosinophil level (PBEL). An atopy-independent association between CC16 38AA and asthma prevalence was identified, suggesting the CC16 38A allele predisposes to adult asthma independent of Th1/Th2 processes. This finding is consistent with previous studies in children, but is the first reported association between CC16 A38G and asthma in adults. CC16 38A also displayed a positive linear trend with atopic dermatitis.
克拉拉细胞16 kDa(CC16)蛋白基因是哮喘易感性的一个很有前景的候选基因。CC16 38A等位基因与澳大利亚儿童血浆CC16水平降低及哮喘发病率增加有关。迄今为止,这些结果在成年人中尚未得到重复验证。因此,在未经过挑选的年轻丹麦成年人人群中,对CC16 A38G、哮喘和特应性之间的潜在联系进行了研究。464名来自哥本哈根、年龄在19至29岁之间的丹麦人参与了一项哮喘和过敏表型-基因型研究。通过对跨越A38G多态性的PCR产物进行Sau96I限制性消化来进行基因分型。使用回归分析研究潜在的A38G基因型与哮喘相关表型的关联,并在适当情况下对潜在混杂因素进行校正。与具有38GG基因型的成年人相比,具有38AA基因型的成年人当前患哮喘的几率更高(比值比3.2,P = 0.013),既往患哮喘的几率也更高(比值比2.2,P = 0.045)。校正特应性对这种关系的影响最小。38A等位基因与特应性皮炎之间存在明显的正线性趋势(比值比1.67,P = 0.02)。未发现A38G多态性与鼻炎、特应性、1秒用力呼气量(FEV(1))、用力肺活量(FVC)、对组胺的气道反应性(AR)或外周血嗜酸性粒细胞水平(PBEL)之间存在关联。确定了CC16 38AA与哮喘患病率之间存在不依赖特应性的关联,这表明CC16 38A等位基因使成年人易患哮喘,且独立于Th1/Th2过程。这一发现与之前对儿童的研究一致,但却是首次报道CC16 A38G与成年人哮喘之间的关联。CC16 38A与特应性皮炎也呈现出正线性趋势。