Oral Pathobionts Promote MS-like Symptoms in Mice

Oral Pathobionts Promote MS-like Symptoms in Mice
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口腔致病生物促进小鼠出现多发性硬化症样症状

DOI:
10.1177/00220345221128202
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发表时间:
2022-10
影响因子:
7.6
通讯作者:
Sheng-Zhong Duan
Sheng-Zhong Duan
中科院分区:
医学1区
文献类型:
--
作者:
Lu-Jun Zhou;Wen-Zhen Lin;Ting Liu;Bo-Yan Chen;Xiao-Qian Meng;Yu-Lin Li;Lin-Juan Du;Yan Liu;You-Cun Qian;Ya-Qin Zhu;Sheng-Zhong Duan

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口腔微生物群失调与多发性硬化症有关。然而,口腔微生物群在多发性硬化症发展中的作用和机制尚不清楚。在这里,我们证明了结合力诱导的牙周炎(LIP)加重了小鼠的实验性自身免疫性脑脊髓炎(EAE),这可能依赖于T辅助17 (Th17)细胞的扩增。LIP增加了肠杆菌的脾脏丰富度,可诱导小鼠脾脏Th17细胞扩增,加重EAE。LIP还导致EAE小鼠肠道内丹毒杆菌(erysipelotricaceae sp.)的富集和大肠固有层中Th17细胞的增加。从患有LIP的EAE小鼠中移植粪便微生物群也能促进EAE症状。总之,牙周炎加重了EAE,可能是通过口腔病原体的异位定植和Th17细胞的扩增。
Dysbiotic oral microbiota has been associated with multiple sclerosis. However, the role and mechanism of oral microbiota in the development of multiple sclerosis are still elusive. Here, we demonstrated that ligature-induced periodontitis (LIP) aggravated experimental autoimmune encephalomyelitis (EAE) in mice, and this was likely dependent on the expansion of T helper 17 (Th17) cells. LIP increased the splenic richness of Enterobacter sp., which was able to induce the expansion of splenic Th17 cells and aggravate EAE in mice. LIP also led to enrichment of Erysipelotrichaceae sp. in the gut and increased Th17 cells in the large intestinal lamina propria of EAE mice. Fecal microbiota transplantation from EAE mice with LIP also promoted EAE symptoms. In conclusion, periodontitis exacerbates EAE, likely through ectopic colonization of oral pathobionts and expansion of Th17 cells.
DOI: 10.1126/science.aan4526
发表时间: 2017-10-20
期刊: Science (New York, N.Y.)
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DOI: 10.1371/journal.pone.0260384
发表时间: 2021
期刊: PloS one
影响因子: 3.7
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DOI: 10.1016/j.celrep.2019.09.002
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期刊: CELL REPORTS
影响因子: 8.8
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DOI: 10.1016/j.jtauto.2020.100039
发表时间: 2020-01-01
影响因子: 3.9
作者:
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通讯作者: Cavallo, Salvatore