口腔致病共生菌会在小鼠中引发类多发性硬化症状。

Oral Pathobionts Promote MS-like Symptoms in Mice.

作者信息

Zhou L-J, Lin W-Z, Liu T, Chen B-Y, Meng X-Q, Li Y-L, Du L-J, Liu Y, Qian Y-C, Zhu Y-Q, Duan S-Z

机构信息

Department of General Dentistry, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

J Dent Res. 2023 Feb;102(2):217-226. doi: 10.1177/00220345221128202. Epub 2022 Oct 20.

DOI:10.1177/00220345221128202

PMID:36266965

Abstract

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 sp., which was able to induce the expansion of splenic Th17 cells and aggravate EAE in mice. LIP also led to enrichment of 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.

摘要

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仍不清楚。在这里，我们证明结扎诱导的牙周炎（LIP）会加重小鼠的实验性自身免疫性脑脊髓炎（EAE），这可能依赖于辅助性T细胞17（Th17）的扩增。LIP增加了某菌属在脾脏中的丰度，该菌属能够诱导脾脏Th17细胞扩增并加重小鼠的EAE。LIP还导致肠道中某菌属富集，并增加EAE小鼠大肠固有层中的Th17细胞。来自患有LIP的EAE小鼠的粪便微生物群移植也会促进EAE症状。总之，牙周炎可能通过口腔致病共生菌的异位定植和Th17细胞的扩增来加重EAE。