Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Department of Pediatrics, Pusan National University Yangsan Hospital, Yangsan, Korea.
Ann Allergy Asthma Immunol. 2014 Aug;113(2):160-165.e1. doi: 10.1016/j.anai.2014.05.019. Epub 2014 Jun 24.
Antibiotic use in infancy induces alteration in intestinal microbiota and is associated with the development of allergic diseases. Mold exposure is also associated with allergic diseases. Genetic susceptibility may interact with specific environmental factors in allergic disease development.
To investigate independent and combined effects of antibiotic use and mold exposure in infancy on the risk of allergic rhinitis (AR) in adolescents.
Data on AR and environmental factors were collected using the International Study of Asthma and Allergies in Childhood questionnaire from 7,389 adolescents from Seoul, Korea. TaqMan genotyping was performed for interleukin 13 (IL-13) (rs20541) and Toll-like receptor 4 (rs1927911) polymorphisms in 1,395 adolescents.
Age, parental history of AR, antibiotic use in infancy, and pet ownership during pregnancy or infancy were associated with an increased risk of current AR (diagnosis of AR and symptoms of AR within the preceding 12 months). Having older siblings was a protective effect. The adjusted odds ratio (aOR) for current AR for combined antibiotic use and mold exposure in infancy was 1.45 (95% confidence interval [CI], 1.01-2.09). For each factor separately, aORs were 1.25 (95% CI, 1.04-1.50) and 0.99 (95% CI, 0.75-1.31), respectively. Antibiotic and mold exposure in infancy, GA or AA genotypes of IL-13 (rs20541) (aOR 4.53; 95% CI, 1.66-12.38; P for interaction = .05), and CT+TT genotype of Toll-like receptor 4 (rs1927911) (aOR, 3.20; 95% CI, 1.24-8.26; P for interaction = .18) increased the risk of current AR.
Antibiotic use and mold exposure in infancy have additive effects on the risk of current AR in genetically susceptible adolescents. Gene-environment interactions between IL-13 (rs20541) and antibiotics or mold may play a role in AR.
婴儿时期使用抗生素会改变肠道微生物群，并与过敏性疾病的发展相关。霉菌暴露也与过敏性疾病相关。遗传易感性可能与过敏性疾病发展过程中的特定环境因素相互作用。
研究婴儿期使用抗生素和霉菌暴露对青少年过敏性鼻炎（AR）风险的独立和联合影响。
使用来自韩国首尔的 7389 名青少年的国际儿童哮喘和过敏研究（ISAAC）问卷调查过敏性鼻炎和环境因素的数据。在 1395 名青少年中进行 TaqMan 基因分型，检测白细胞介素 13（IL-13）（rs20541）和 Toll 样受体 4（rs1927911）多态性。
年龄、父母的 AR 病史、婴儿期使用抗生素和怀孕期间或婴儿期养宠物与当前 AR（AR 的诊断和过去 12 个月内的 AR 症状）的风险增加相关。有年龄较大的兄弟姐妹则是一种保护作用。婴儿期同时使用抗生素和接触霉菌与当前 AR 的调整后比值比（aOR）为 1.45（95%置信区间[CI]，1.01-2.09）。单独考虑每个因素时，aOR 分别为 1.25（95%CI，1.04-1.50）和 0.99（95%CI，0.75-1.31）。婴儿期使用抗生素和接触霉菌、白细胞介素 13（rs20541）GA 或 AA 基因型（aOR 4.53；95%CI，1.66-12.38；P 交互作用=.05）和 Toll 样受体 4（rs1927911）CT+TT 基因型（aOR，3.20；95%CI，1.24-8.26；P 交互作用=.18）增加了当前 AR 的风险。
婴儿期使用抗生素和接触霉菌对遗传易感青少年当前 AR 的风险有相加作用。白细胞介素 13（rs20541）与抗生素或霉菌之间的基因-环境相互作用可能在 AR 中起作用。
