Ahn Jae-Rin, Lee Seung-Hwa, Kim Byunghyun, Nam Myung Hee, Ahn Yoon Kyung, Park Yoon Mee, Jeong Seon-Mi, Park Min Jee, Song Kun Baek, Lee So-Yeon, Hong Soo-Jong
Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea.
Korea Basic Science Institute, Seoul Center, Seoul, Korea.
Pediatr Allergy Immunol. 2022 Jan;33(1):e13678. doi: 10.1111/pai.13678. Epub 2021 Oct 23.
Ruminococcus gnavus (R. gnavus) are mucin-degrading gut bacteria that play a key role in the early colonization of the gut by serving as endogenous sources of nutrients. They can also influence immune development. We had previously reported a lower abundance of R. gnavus in infants with atopic dermatitis (AD) compared with that in healthy subjects. However, the underlying mechanisms remain unclear. In this study, we investigated the effect of orally administered R. gnavus on antibiotic treatment-induced gut dysbiosis (and the underlying mechanism) in a mouse model of AD.
Four-week-old female BALB/C mice were administered antibiotic cocktails for 2 weeks. R. gnavus was orally administered throughout the study duration. At 6 weeks of age, AD was induced by epidermal sensitization with ovalbumin. AD phenotypes and systemic and gut immune responses were investigated.
Orally administered R. gnavus significantly reduced AD-associated parameters (i.e., transepidermal water loss, clinical score, total serum immunoglobulin (Ig) E level, OVA-specific IgE level, and skin inflammation). R. gnavus treatment also resulted in significant downregulation of T helper 2-related cytokine mRNA and upregulation of interleukin (IL)-10 and Foxp3 in the skin. The population of CD4 FOXP3 T cells in mesenteric- and skin-draining lymph nodes and butyrate levels in the cecum increased in R. gnavus-administered AD mice.
Immune modulation by orally administered R. gnavus may alleviate AD symptoms through the enhancement of regulatory T-cell counts and short-chain fatty acids production in AD mice.
迟缓瘤胃球菌是一种可降解黏蛋白的肠道细菌，作为内源性营养来源，在肠道早期定植过程中发挥关键作用。它们还能影响免疫发育。我们之前报道过，与健康受试者相比，特应性皮炎（AD）婴儿体内的迟缓瘤胃球菌丰度较低。然而，其潜在机制仍不清楚。在本研究中，我们在AD小鼠模型中研究了口服迟缓瘤胃球菌对抗生素治疗引起的肠道菌群失调（及其潜在机制）的影响。
给4周龄雌性BALB/C小鼠服用抗生素鸡尾酒2周。在整个研究期间口服迟缓瘤胃球菌。6周龄时，通过卵清蛋白进行表皮致敏诱导AD。研究了AD表型以及全身和肠道免疫反应。
口服迟缓瘤胃球菌显著降低了与AD相关的参数（即经表皮水分流失、临床评分、血清总免疫球蛋白（Ig）E水平、OVA特异性IgE水平和皮肤炎症）。迟缓瘤胃球菌治疗还导致皮肤中辅助性T细胞2相关细胞因子mRNA显著下调，白细胞介素（IL）-10和Foxp3上调。在口服迟缓瘤胃球菌的AD小鼠中，肠系膜和皮肤引流淋巴结中的CD4 FOXP3 T细胞数量以及盲肠中的丁酸盐水平增加。
口服迟缓瘤胃球菌的免疫调节作用可能通过增加AD小鼠体内调节性T细胞数量和短链脂肪酸生成来减轻AD症状。
