唾液外基因组通过桥梁口腔和肠道加剧结肠炎
Congyi Yang1, Jingyi Chen1, Yuzheng Zhao1
1Department of Gastroenterology, Peking University People's Hospital, Beijing 100044, China.
iScience
|January 6, 2025
概括
来自活跃炎症性肠病 (IBD) 患者的唾液衍生外体会在小鼠中恶化结肠炎. 这些外体对肠道炎症产生影响,这表明口腔健康和IBD进展之间存在联系.
科学领域:
- 胃肠道学和免疫学
- 口腔医学是指口腔医学.
- 异构体生物学 异构体生物学
背景情况:
- 炎症性肠病 (IBD) 与肠外表现有关,包括口腔问题.
- 在IBD中口腔肠交叉的精确机制仍然不完全理解.
- 唾液外体在IBD病原体中的作用需要进一步研究.
研究的目的:
- 在IBD的背景下研究唾液外体的功能作用.
- 探索IBD活跃患者对外体对大肠炎的影响,与缓解期患者对大肠炎的影响.
- 阐明唾液外对肠道炎症影响的潜在机制.
主要方法:
- 使用硫酸德克斯 (DSS) 的大肠炎小鼠模型.
- 从活跃IBD患者 (活跃IBD-Sexos) 和缓解IBD患者 (缓解IBD-Sexos) 给小鼠的唾液外体.
- 在体外与THP-1 (巨) 和Caco-2 (肠上皮) 细胞进行了共同培养实验.
- 在活性IBD-Sexos中分析了差异表达的microRNA (miRNA).
主要成果:
- 在DSS小鼠模型中,活性IBD-Sexos显著加剧了结肠炎.
- 缓解IBD-Sexos对结肠炎没有类似的恶化作用.
- 实验室研究表明,THP-1细胞中的IBD-Sexos诱导的炎症反应活跃,Caco-2细胞中的紧结蛋白表达减少.
- 在活性IBD-Sexos中鉴定了35个差异表达的miRNA.
结论:
- 活跃IBD患者的唾液外基因组可以使实验性结肠炎恶化,突出显示潜在的口腔肠轴机制.
- 活性IBD-Sexos可能通过巨分化,肠上皮质屏障破坏和肠道微生物群变化影响结肠炎.
- 这些发现强调了唾液外体的作用,即作为IBD相关的口腔肠交叉通道中介的媒介.
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