减少的SCFA产生肠道微生物参与了川崎病的炎症激活
Fangyan Wang1,2, Fanyu Qian3,4, Qihao Zhang3,5
1Department of Pathophysiology, School of Basic Medical Science, Wenzhou Medical University, Wenzhou, China.
Frontiers in immunology
|July 3, 2023
概括
川崎病 (KD) 涉及改变的肠道细菌,减少有益的短链脂肪酸 (SCFA). 益生菌治疗改善了肠道健康,并减少了小鼠模型中的炎症,这表明了对KD的新治疗方法.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 儿童心脏病学 儿童心脏病学
背景情况:
- 川崎病 (KD) 是儿童获得心脏病的主要原因.
- 在急性阶段,在KD患者中观察到肠道微生物组合的改变.
- 肠道失生症在KD病变发生过程中的特定作用仍然在很大程度上是未知的.
研究的目的:
- 在KD小鼠模型中研究肠道微生物群的特征.
- 探索使用益生菌或抗生素调节肠道微生物群的治疗潜力.
- 阐明涉及短链脂肪酸 (SCFA) 和肠道屏障功能的潜在机制.
主要方法:
- 在小鼠模型中诱导KD.
- 使用益生菌*Clostridium butyricum*和抗生素尾酒来调节肠道微生物群.
- 对肠道微生物群组成和SCFA生产 (GC-MS) 的分析.
- 评估肠道屏障完整性 (蛋白质表达,血D-乳酸盐).
- 评估炎症标志物 (IL-1β,IL-6) 和MAPK信号通路 *在体外*.
主要成果:
- 凯迪小鼠表现出减少的SCFA产生细菌和降低的SCFA水平 (丁酸盐,乙酸盐,酸盐).
- *Clostridium butyricum*治疗恢复了SCFA产生细菌,减轻了冠状动脉病变,并减少了炎症.
- 抗生素治疗加剧了炎症和肠道屏障功能障碍 (克劳丁-1,Jam-1,Occludin,ZO-1的减少;D-乳酸盐的增加).
- 丁酸盐,但不是酸盐或酸盐,通过上调MKP-1表达来抑制*in vitro*的炎症.
结论:
- 肠道功能障碍,以减少SCFA生产和肠道屏障受损为特征,有助于KD的发病.
- 益生菌*Clostridium butyricum*通过恢复肠道微生物群和SCFA水平,显示了对KD的治疗潜力.
- 准肠道微生物群和SCFA生产为KD治疗提供了一种新的策略.
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