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首页> 外文期刊>Allergy >Interaction of a 17q12 variant with both fetal and infant smoke exposure in the development of childhood asthma-like symptoms
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Interaction of a 17q12 variant with both fetal and infant smoke exposure in the development of childhood asthma-like symptoms

机译：17q12变异与胎儿和婴儿烟气暴露在儿童期哮喘样症状发展中的相互作用

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Background Gene variants on chromosome 17q12-21 are associated with an increased risk of childhood-onset asthma, a risk known to be modified by environmental tobacco smoke (ETS). Objectives To assess whether the association of rs2305480 on chromosome 17q12 in the GSDML gene with asthma-like symptoms in the first 4 years of life is modified by smoke exposure during fetal and early postnatal life. Methods We used data from two independent prospective cohort studies from fetal life onwards in the Netherlands. We genotyped rs2305480 and assessed maternal smoking during pregnancy and ETS exposure at the age of 2. Asthma-like symptoms, defined as any reported wheezing, shortness of breath or dry nocturnal cough, were reported by parents when the children were 1, 2, 3, and 4 years. Analyses were based on a total group of 4461 Caucasian children. Results The G risk-allele of rs2305480 was associated with asthma-like symptoms [overall odds ratio 1.17 (1.11, 1.24), 2.66E-9]. The effect of rs2305480 on asthma-like symptoms was stronger among children who were exposed to smoke during fetal life (P-interaction = 0.04). Smoke exposure in early postnatal life was also associated with an increased effect of the 17q12 single nucleotide polymorphism (SNP) on asthma-like symptoms (P-interaction = 5.06E-4). These associations were consistent in both cohorts. Conclusion A 17q12 variant, rs2305480, was associated with asthma-like symptoms in preschool children, and this association was modified by smoke exposure already during fetal life, and in infancy. Further investigation regarding SNPs in linkage disequilibrium with rs2305480 in relation to pathophysiological pathways is needed.
机译：背景染色体17q12-21上的基因变异与儿童哮喘发作的风险增加有关，这种风险已知会被环境烟草烟雾（ETS）改变。目的评估胎儿和出生后早期的烟尘暴露是否能改变GSDML基因17q12染色体rs2305480与生命最初4年的哮喘样症状之间的联系。方法我们使用了来自荷兰从胎儿生命开始的两项独立的前瞻性队列研究的数据。我们对rs2305480进行了基因分型，并评估了孕妇在怀孕期间的吸烟情况以及2岁时的ETS暴露情况。父母在孩子1、2、3岁时报告了哮喘样症状，定义为任何报告的喘息，呼吸急促或夜间咳嗽。和4年。分析基于总共4461名白人儿童的情况。结果rs2305480的G风险等位基因与哮喘样症状相关[总比值比为1.17（1.11、1.24），2.66E-9]。在胎儿生命期间接触烟气的儿童中，rs2305480对哮喘样症状的影响更强（P相互作用= 0.04）。出生后早期吸烟与17q12单核苷酸多态性（SNP）对哮喘样症状的作用增强有关（P-相互作用= 5.06E-4）。这些关联在两个队列中都是一致的。结论17q12变体rs2305480与学龄前儿童的哮喘样症状相关，并且这种关联已通过在胎儿生命中和婴儿期已经暴露于烟雾而得到改善。需要进一步研究与rs2305480连锁不平衡的SNPs相关的病理生理途径。

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