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Bo-Yan Chen^1,2,3,4,5, Hong Zhu^1,3,4,5,6, Yu-Lin Li^3,4,5

¹Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China (B.-Y.C., H.Z., M.Y., Q.C., S.-Z.D.).

|August 27, 2025

概括

牙周炎会通过口腔病原体在心脏中积累而加剧心肌梗塞,从而激活炎症性B2细胞. 针对牙周炎和口腔细菌可以改善心脏病治疗.

科学领域:

心血管研究
微生物学
免疫学

背景情况:

心肌梗塞 (MI) 是全球主要的死亡原因.
牙周炎与肌痛性心脏病有关,但直接影响和机制尚不清楚.
需要阐明口腔病原体在心脏病发作中的作用.

研究的目的:

研究牙周炎对心肌梗塞的直接影响.
识别与恶化心脏病有关的口腔病原体.
探索微生物信号调节MI病变的机制.

主要方法:

用于结合绑定诱导的PD和MI的小鼠模型.
细菌测序和FISH在心脏组织中发现了外宫口腔病原体.
流细胞测量和 gnotobiotic 鼠标实验特征了 B2 细胞反应.
用于机理研究的基因淘汰小鼠菌株和突变细菌菌株.
针对临床相关性,研究人员招募了患有心脏病发作和心脏病发作的人类患者.

主要成果:

在小鼠模型中,牙周炎和口腔病原体加剧了心脏病发作.
鉴定了特定的口腔病原体,包括*Prevotella intermedia*和*Fusobacterium nucleatum*.
这些病原生物在心脏病发作中积累, 损害了上皮和内皮屏障.
口服的病原体调动了促炎B2细胞,增加了心脏病发作的严重程度.
通过S1P-S1PR和CXCL13-CXCR5信号通路,B细胞迁移到心脏.

结论:

口腔病原体和B2细胞显著恶化MI,建立了一个新的口腔-心脏轴.
针对PD,口腔病原体或相关免疫机制的干预措施显示出对MI的治疗潜力.

关键词:

乙淋巴细胞子集心肌梗塞牙周炎

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