IFN-I介导的中性形成偏差驱动中性粒细胞原始化和炎症性并发症
Yuman Li1, Yiming Chen1, Chenyu Deng1
1Department of Geriatric Dentistry, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, 100081, PR China.
Theranostics
|June 16, 2025
概括
牙周炎驱动关节炎,因为它使骨髓细胞的产生偏向于中性粒细胞,这种过程由I型干扰素信号传递介导. 解决牙周炎可以扭转这种偏见,并减少关节炎的严重程度.
科学领域:
- 免疫学 免疫学 免疫学
- 血液学 血液学 血液学
- 牙周病学 牙周病学
背景情况:
- 局部慢性炎症,如牙周炎,与全身性疾病有关.
- 连接牙周炎与关节炎等全身炎症的机制需要进一步阐明.
研究的目的:
- 调查牙周炎如何影响骨髓血质形成,特别是中性质形成.
- 确定中性粒细胞重编程在加剧关节炎中的作用.
主要方法:
- 血造干细胞和原始细胞 (HSPC) 的单细胞多组测序来自带有带诱导牙周炎 (LIP) 的小鼠.
- 对差异化轨迹,转录因子和中性粒细胞原始化的分析.
- 在原抗体诱导性关节炎模型中对原始中性粒细胞的功能性评估.
- 询问I型干扰素 (IFN-I) 信号通路和检查牙周炎的解决方案.
主要成果:
- 在HSPC分化中,LIP诱导了偏差,有利于中性粒细胞系,导致扩大原始中性粒细胞.
- 原始化的中性粒细胞加剧了远端关节炎.
- 在HSPC中IFN-I信号的升高驱动了中性质形成偏差.
- 牙周炎的解决逆转了造血偏差和减轻了关节炎.
结论:
- 牙周炎通过IFN-I介导的中性质形成偏差使关节炎恶化.
- 控制局部慢性炎症对于管理系统性炎症并发症至关重要.
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