한빛사 논문
Min-Jung Leea, Yoon Mee Parkb, Byunghyun Kimc, in Hwan Taec, Nam-Eun Kimd, Marina Pranatae, Taewon Kimf, Sungho Wond, Nam Joo Kangf,g, Yun Kyung Leee, Dong-Woo Leeh, Myung Hee Namc, Soo-Jong Hongi,* and Bong-Soo Kima,j,*
aDepartment of Life Science, Multidisciplinary Genome Institute, Hallym University, Chuncheon, Republic of Korea; bAsan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea; cSeoul Center, Korea Basic Science Institute, Seoul, Republic of Korea; dDepartment of Public Health Sciences, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea; eDepartment of Integrated Biomedical Science, Soonchunhyang Institute of Medi-Bioscience, Soonchunhyang University, Cheonan, Republic of Korea; fSchool of Food Science and Biotechnology, Kyungpook National University, Daegu, Republic of Korea; gDepartment of Integrative Biology, Kyungpook National University, Daegu, Republic of Korea; hDepartment of Biotechnology, Yonsei University, Seoul, Republic of Korea; iDepartment of Pediatrics, Childhood Asthma Atopy Center, Humidifier Disinfectant Health Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; jThe Korean Institute of Nutrition, Hallym University, Chuncheon, Republic of Korea
*Corresponding author.
Abstract
The gut microbiome influences the development of allergic diseases during early childhood. However, there is a lack of comprehensive understanding of microbiome-host crosstalk. Here, we analyzed the influence of gut microbiome dynamics in early childhood on atopic dermatitis (AD) and the potential interactions between host and microbiome that control this homeostasis. We analyzed the gut microbiome in 346 fecal samples (6–36 months; 112 non-AD, 110 mild AD, and 124 moderate to severe AD) from the Longitudinal Cohort for Childhood Origin of Asthma and Allergic Disease birth cohort. The microbiome-host interactions were analyzed in animal and in vitro cell assays. Although the gut microbiome maturated with age in both AD and non-AD groups, its development was disordered in the AD group. Disordered colonization of short-chain fatty acids (SCFA) producers along with age led to abnormal SCFA production and increased IgE levels. A butyrate deficiency and downregulation of GPR109A and PPAR-γ genes were detected in AD-induced mice. Insufficient butyrate decreases the oxygen consumption rate of host cells, which can release oxygen to the gut and perturb the gut microbiome. The disordered gut microbiome development could aggravate balanced microbiome-host interactions, including immune responses during early childhood with AD.
논문정보
관련 링크
관련분야 연구자보기
관련분야 논문보기
해당논문 저자보기