乳酸菌肠道 (Lactobacillus Intestinalis) 促使上皮细胞通过宿主-微生物视网膜酸生物合成来抑制结肠炎相关的Th17反应
Qi-Wen Wang1, Ding-Jia-Cheng Jia2, Jia-Min He1
1Department of Gastroenterology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, Zhejiang, 310058, China.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|November 20, 2023
概括
一种新型益生菌Lactobacillus intestinalis通过向Th17细胞,显示出对小鼠的性结肠炎的保护作用. 这种益生菌调节肠道上皮质免疫反应,对炎症性肠道疾病具有潜在的治疗益处.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 性结肠炎 (UC) 的发病与肠道微生物群密切相关.
- Th17细胞在UC相关的炎症中起着至关重要的作用.
研究的目的:
- 在大肠炎的小鼠模型中研究Lactobacillus intestinalis (L. intestinalis) 的治疗潜力.
- 阐明L. intestinalis的保护作用背后的机制.
主要方法:
- 在小鼠中使用德克斯硫酸盐 (DSS) 诱导的大肠炎模型.
- 流细胞计分析T助手17 (Th17) 细胞.
- 对表皮SAA1/SAA2产生和视网膜酸 (RA) 生物合成的分析.
- 在UC患者中评估L. intestinalis的丰度.
主要成果:
- L. intestinalis 显示出对DSS诱导的大肠炎具有显著的保护作用.
- 保护作用依赖于T细胞和IL-17A,而L. intestinalis的目标是Th17细胞.
- L. intestinalis 减少了表皮SAA1/SAA2 生产,并通过ALDH和ALDH1A2 彗代谢通过RAR-α调解增加了网膜酸 (RA) 生物合成.
- 在UC患者中,便L. intestinalis的丰度与C/EBPA-SAA1/2-Th17轴负相关.
- 在缓解大肠炎方面,L. intestinalis与梅萨拉具有协同作用.
结论:
- 在性结肠炎中,L. intestinalis具有治疗潜力.
- 它的机制涉及通过减少SAA产生和增加RA生物合成来调节上皮-免疫交叉,从而抑制Th17介导的炎症.
- L. intestinalis及其代谢物RA是UC治疗的有希望的候选者.
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