牙周炎
变形链球菌
失调
神经退行性变
神经炎症
多巴胺能
生物
免疫学
病理
医学
肠道菌群
内科学
多巴胺
内分泌学
炎症
疾病
遗传学
细菌
作者
Xuebing Bai,Shuo Xu,Lu‐Jun Zhou,Xiao-Qian Meng,Yulin Li,Yanlin Chen,Yijie Jiang,Wei-Ming Lin,Bo‐Yan Chen,Lin‐Juan Du,Guocai Tian,Yan Liu,Sheng-Zhong Duan,Yaqin Zhu
出处
期刊:Microbiome
[Springer Nature]
日期:2023-11-17
卷期号:11 (1)
标识
DOI:10.1186/s40168-023-01685-w
摘要
Parkinson's disease (PD) is a common chronic neurological disorder with a high risk of disability and no cure. Periodontitis is an infectious bacterial disease occurring in periodontal supporting tissues. Studies have shown that periodontitis is closely related to PD. However, direct evidence of the effect of periodontitis on PD is lacking. Here, we demonstrated that ligature-induced periodontitis with application of subgingival plaque (LIP-SP) exacerbated motor dysfunction, microglial activation, and dopaminergic neuron loss in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice.The 16S rRNA gene sequencing revealed that LIP-SP induced oral and gut dysbiosis. Particularly, Veillonella parvula (V. parvula) and Streptococcus mutans (S. mutans) from oral ligatures were increased in the fecal samples of MPTP + LIP-SP treated mice. We further demonstrated that V. parvula and S. mutans played crucial roles in LIP-SP mediated exacerbation of motor dysfunction and neurodegeneration in PD mice. V. parvula and S. mutans caused microglial activation in the brain, as well as T helper 1 (Th1) cells infiltration in the brain, cervical lymph nodes, ileum and colon in PD mice. Moreover, we observed a protective effect of IFNγ neutralization on dopaminergic neurons in V. parvula- and S. mutans-treated PD mice.Our study demonstrates that oral pathogens V. parvula and S. mutans necessitate the existence of periodontitis to exacerbate motor dysfunction and neurodegeneration in MPTP-induced PD mice. The underlying mechanisms include alterations of oral and gut microbiota, along with immune activation in both brain and peripheral regions. Video Abstract.
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