牙周炎通过通过肠道微生物介导的抑制GPR109A促进肠道炎症
Xinyue Wang1, Zhonghan Xu1, Yujie Yao1
1Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Frontiers in cellular and infection microbiology
|March 12, 2026
概括
牙周炎通过通过肠道微生物群减少GPR109A受体表达而导致肠道炎症. 激活这种受体可以恢复肠道屏障功能,并减少炎症.
科学领域:
- 胃肠病学 胃肠病学
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 牙周炎是一种慢性炎症性疾病,与全身性疾病有关.
- 肠道微生物群在维持肠道平衡和免疫功能方面发挥着至关重要的作用.
- GPR109A (尼亚受体1) 在结肠表达,具有抗炎性质.
研究的目的:
- 调查牙周炎在促进肠道炎症中的作用.
- 为了确定肠道微生物是否通过抑制GPR109A受体来调解这种效应.
- 探索针对GPR109A.的治疗策略.
主要方法:
- 在小鼠中诱导牙周炎,并评估结肠GPR109A表达,肠道屏障完整性和炎症标志物.
- 分析了肠道微生物群的组成和功能,包括短链脂肪酸的产生.
- 用便微生物种植和GPR109A激活来确定因果关系和测试干预措施.
主要成果:
- 牙周炎显著降低了结肠GPR109A的表达,并破坏了肠道屏障蛋白 (ZO-1,Occludin).
- 由牙周炎诱导的小鼠的肠道微生物群将炎症表型和GPR109A抑制转移到无菌接受者.
- 激活GPR109A逆转了屏障破坏,并降低了促炎性细胞因子水平.
结论:
- 牙周炎通过肠道微生物群诱导的GPR109A抑制促进肠道炎症.
- 这种抑制导致肠道上皮屏障的破坏.
- 激活GPR109A是一种潜在的治疗策略,可以恢复屏障功能并减少肠道炎症.
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