肠道微生物衍生代谢物通过调节皮肤Th17细胞驱动牛皮炎
Chenliang Wang1, Shangzhi Dai2, Shanshan Zhang3
1Institute for Immunology, School of Basic Medical Sciences, Tsinghua University, Beijing 100084, China; Tsinghua-Peking Center for Life Sciences, Beijing 100084, China.
Immunity
|September 10, 2025
概括
肠道微生物产生的英多尔驱动牛皮炎通过增加硫酸 (I3S). 这种代谢物通过烯碳水化合物受体 (AHR) 发出信号,恶化皮肤炎症,与人类的疾病严重程度相关.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 代谢学 代谢学 代谢学
背景情况:
- 在像牛皮这样的疾病中,慢性炎症涉及复杂的遗传和环境相互作用.
- 维持慢性皮肤病理的确切机制,如牛皮,仍然不完全理解.
研究的目的:
- 研究肠道微生物群,全身代谢物和皮肤炎症在牛皮小鼠模型中的发展之间的联系.
- 阐明微生物代谢物在增强牛皮病理中的机械作用.
主要方法:
- 利用卡14E138A/+的小鼠模型来研究自发性皮肤炎症.
- 分析了皮肤免疫架构和系统代谢物的变化.
- 采用技术识别肠道微生物驱动因素及其代谢产品.
- 研究了皮肤T助手17 (Th17) 细胞中涉及酸 (I3S) 和酸受体 (AHR) 的信号通路.
- 与人类牛皮队伍相关的发现.
主要成果:
- 在小鼠模型中,自发性皮肤炎症改变了皮肤免疫力和全身代谢.
- 鉴定出产的肠道微生物群,而不是皮肤微生物群,是牛皮炎炎的关键驱动因素.
- 一个涉及肠道微生物的代谢继电器导致宿主硫酸 (I3S) 生物合成的增加.
- I3S通过皮肤T助手17 (Th17) 细胞的烯碳水化合物受体 (AHR) 作用,增强染色质的可访问性和炎症.
- 人类牛皮患者血清I3S水平升高与疾病严重程度有显著的相关性.
结论:
- 建立了肠道微生物代谢物和牛皮的皮肤炎症之间的机械联系.
- 确定了一种新的途径,其中肠道衍生的硫酸 (I3S) 通过Th17细胞中的AHR信号来加剧皮肤炎症.
- 突出了肠道微生物群及其代谢物,作为治疗牛皮的潜在治疗点.
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