| Author |
Yang, Song-I Lee, Eun Jung, Young-Ho Kim, Hyung Young Seo, Ju-Hee Kwon, Ji-Won Kim, Byoung-Ju Kim, Hyo-Bin Lee, So-Yeon Jang, Gwang Cheon Kim, Woo-Kyung Shim, Jung Yeon Kang, Mi-Jin Yu, Ho-Sung Hong, Soo-Jong |
| Description |
Author Affiliation: Yang SI ( 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.); Lee E ( 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.); Jung YH ( 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.); Kim HY ( Department of Pediatrics, Pusan National University Yangsan Hospital, Yangsan, Korea.); Seo JH ( Department of Pediatrics, Korea Cancer Center Hospital, Seoul, Korea.); Kwon JW ( Department of Pediatrics, Seoul National University Bundang Hospital, Seungnam, Korea.); Kim BJ ( Department of Pediatrics, Inje University Haeundae Paik Hospital, Busan, Korea.); Kim HB ( Department of Pediatrics, Inje University Sanggye Paik Hospital, Seoul, Korea.); Lee SY ( Department of Pediatrics, Hallym Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea.); Jang GC ( Department of Pediatrics, National Health Insurance Corporation Ilsan Hospital, Goyang, Korea.); Kim WK ( Department of Pediatrics and the Allergy and Respiratory Research Laboratory, Inje University Seoul Paik Hospital, Seoul, Korea.); Shim JY ( Department of Pediatrics, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.); Kang MJ ( Asan Institute for Life Science, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.); Yu HS ( Asan Institute for Life Science, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.); Hong SJ ( 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. Electronic address: sjhong@amc.seoul.kr.) |
| Abstract |
BACKGROUND: 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. OBJECTIVE: To investigate independent and combined effects of antibiotic use and mold exposure in infancy on the risk of allergic rhinitis (AR) in adolescents. METHODS: 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. RESULTS: 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. CONCLUSION: 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. |
