牙周炎的唾液微生物群加剧了由肠道微生物群诱导的巨细胞衍生的CXCL3引起的结肠炎
Jun Qian1, Qing Tao2,3, Yue Shen1
1Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Microbiome
|December 10, 2025
概括
牙周炎的唾液微生物群通过改变肠道细菌和增加巨细胞的CXCL3分泌来恶化结肠炎. 像Lactobacillus rhamnosus GG这样的益生菌可以帮助管理这种情况.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
背景情况:
- 口腔肠轴在结肠炎的发展中起着至关重要的作用.
- 唾液中的口腔细菌可以影响肠道微生物群和结肠炎,但机制尚不清楚.
研究的目的:
- 研究肠道微生物群在唾液微生物群影响的结肠炎中的作用和机制.
- 探索牙周炎唾液微生物群 (PSM) 如何影响大肠炎.
主要方法:
- 结肠炎严重程度与牙周炎唾液微生物群 (PSM) 与健康的唾液微生物群 (HSM) 的比较.
- 对肠道微生物群组成和关键介质的分析,如C-X-C动机化学因子连接体3 (CXCL3).
- 研究了Lactobacillus rhamnosus GG作为潜在的治疗干预措施的影响.
主要成果:
- 与HSM相比,PSM显著加剧了结肠炎,这种效应被抗生素逆转,表明有病原性肠道微生物群.
- PSM导致肠道病原体 (例如大肠杆菌) 和脂多糖的增加,通过CXCL3.3促进大肠炎.
- 由PSM衍生的肠道微生物群在巨细胞中调节了CXCL3,这通过中性粒细胞化学反应和M2b类巨细胞极化促进了大肠炎.
结论:
- 肠道微生物群是PSM恶化的结肠炎的关键因素,由巨细胞激活和CXCL3分泌介导.
- 这项研究阐明了肠道微生物群,巨细胞和大肠炎中的化学因子之间的相互作用.
- 研究结果提供了关于口腔疾病如何系统地影响远端器官的见解.
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