Chun Jaemoo, Lee So Min, Ahn You Mee, Baek Min-Gyung, Yi Hana, Shin Sarah, Jung Jeeyoun
KM Science Research Division, Korea Institute of Oriental Medicine, Daejeon, South Korea.
KM Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon, South Korea.
Front Pharmacol. 2021 Sep 20;12:722730. doi: 10.3389/fphar.2021.722730. eCollection 2021.
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by complex immune dysregulation and closely related to the gut microbiome. The present study investigated the microbiome-mediated effect of (SHCGT) on AD-like symptoms induced by 2,4-dinitrochlorobenzene (DNCB) in BALB/c mice. DNCB was applied regularly to the ear and dorsal skin of BALB/c mice, and SHCGT was administered orally daily for 2 weeks. The composition of the gut microbiota was analyzed using 16S rRNA sequencing, and the effect of gut microbiome-derived metabolites, specifically short-chain fatty acids (SCFAs), was evaluated in tumor necrosis factor-alpha (TNF-α)- and interferon-gamma (IFN-γ)-treated HaCaT cells. SHCGT alleviated DNCB-induced symptoms of AD and the immune response to AD by decreasing the plasma immunoglobulin E level and splenic interleukin-4, interleukin-10, TNF-α, and IFN-γ levels. The gut microbiome composition and the damaged gut epithelial barrier in mice with AD were also significantly altered by SHCGT, and the reduced SCFA levels therein were elevated. We found that SFCAs directly inhibited the mRNA expression of IL-6 and ICAM-1 in TNF-α- and INF-γ-treated HaCaT cells. The finding that SHCGT regulates the gut microbiome and improves DNCB-induced AD in mice suggests that this herbal medicine has therapeutic potential in patients with AD.
特应性皮炎（AD）是一种慢性炎症性皮肤病，其特征为复杂的免疫失调，且与肠道微生物群密切相关。本研究调查了（此处SHCGT不完整，请补充完整准确名称）对2,4-二硝基氯苯（DNCB）诱导的BALB/c小鼠AD样症状的微生物群介导作用。将DNCB定期涂抹于BALB/c小鼠的耳部和背部皮肤，并每天口服（此处SHCGT不完整，请补充完整准确名称），持续2周。使用16S rRNA测序分析肠道微生物群的组成，并在肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）处理的HaCaT细胞中评估肠道微生物群衍生代谢物，特别是短链脂肪酸（SCFAs）的作用。（此处SHCGT不完整，请补充完整准确名称）通过降低血浆免疫球蛋白E水平以及脾脏白细胞介素-4、白细胞介素-10、TNF-α和IFN-γ水平，减轻了DNCB诱导的AD症状和对AD的免疫反应。（此处SHCGT不完整，请补充完整准确名称）还显著改变了AD小鼠的肠道微生物群组成和受损的肠道上皮屏障，并提高了其中降低的SCFA水平。我们发现，SCFAs直接抑制了TNF-α和INF-γ处理的HaCaT细胞中IL-6和ICAM-1的mRNA表达。（此处SHCGT不完整，请补充完整准确名称）调节肠道微生物群并改善DNCB诱导的小鼠AD这一发现表明，这种草药对AD患者具有治疗潜力。
