Kang Mi Jin, Lee So Yeon, Park Yoon Mee, Kim Bong Soo, Lee Min Jung, Kim Jeong Hyun, Jeong Seonmi, Lee Seung Hwa, Park Min Jee, Rhee Eun Sang, Jung Sungsu, Yoon Jisun, Cho Hyun Ju, Lee Eun, Yang Song I, Suh Dong In, Kim Kyung Won, Sheen Youn Ho, Ahn Kangmo, Hong Soo Jong
Humidifier Disinfectant Health Center, Asan Medical Center, Seoul, Korea.
Department of Pediatrics, Childhood Asthma Atopy Center, Humidifier Disinfectant Health Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Allergy Asthma Immunol Res. 2021 May;13(3):404-419. doi: 10.4168/aair.2021.13.3.404.
Interleukin (IL)-17 variants and perturbations in the gut microbiota may influence the development of atopic dermatitis (AD). However, unifying principles for variants of host and microbe interaction remains unclear. We sought to investigate whether variants and gut microbiota affect the development of AD in infancy.
Composition of the gut microbiota was analyzed in fecal samples from 99 normal healthy and 61 AD infants at 6 months of age. The associations between total immunoglobulin E (IgE), the scoring atopic dermatitis (SCORAD), short-chain fatty acids, transcriptome and functional profile of the gut measured in these subjects and were analyzed. IL-6 and IL-8 in the human intestinal epithelial cell line (HIEC-6) were measured after stimulation of IL-17 and .
In this study, was enriched in infants with AD and was higher in those with the GA + AA of (rs2275913) variant. was positively correlated with IgE and SCORAD in infants with AD and GA + AA of . Butyrate and valerate were negatively correlated with and were decreased in infants with AD and GA + AA. Bacterial genes for oxidative phosphorylation induced by reduced colonization of were decreased compared with normal and GG. In transcriptome analysis, lactate dehydrogenase A-like 6B was higher in infants with AD compared with healthy infants. IL-6 and IL-8 were increased in IL-17 and/or -stimulated HIEC-6 cells.
These findings suggest that increased and A allele of (rs2275913) may contribute to the pathogenesis of AD via modulation of the immune system in infancy.
白细胞介素（IL）-17变体与肠道微生物群的紊乱可能会影响特应性皮炎（AD）的发展。然而，宿主与微生物相互作用变体的统一原理仍不清楚。我们试图研究这些变体和肠道微生物群是否会影响婴儿期AD的发展。
分析了99名正常健康婴儿和61名AD婴儿6个月大时粪便样本中的肠道微生物群组成。分析了这些受试者中测量的总免疫球蛋白E（IgE）、特应性皮炎评分（SCORAD）、短链脂肪酸、肠道转录组和功能谱之间的关联。在刺激IL-17和 后，测量人肠道上皮细胞系（HIEC-6）中的IL-6和IL-8。
在本研究中， 在AD婴儿中富集，在携带 （rs2275913）变体GA + AA的婴儿中更高。 在AD婴儿和携带GA + AA的婴儿中与IgE和SCORAD呈正相关。丁酸盐和戊酸盐与 呈负相关，在AD婴儿和携带GA + AA的婴儿中减少。与正常和GG相比，因 定殖减少而诱导的氧化磷酸化细菌基因减少。在转录组分析中，与健康婴儿相比，AD婴儿中乳酸脱氢酶A样6B更高。在IL-17和/或 刺激的HIEC-6细胞中，IL-6和IL-8增加。
这些发现表明，增加的 和 （rs2275913）的A等位基因可能通过调节婴儿期的免疫系统而导致AD的发病机制。
