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Oral Pathobionts Promote MS-like Symptoms in Mice
L-J Zhou1,2,3, W-Z Lin1,2,3, T Liu2,3
1Department of General Dentistry, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
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 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.
Insights
Periodontitis, an oral condition, worsens multiple sclerosis models in mice by promoting specific gut bacteria. This oral dysbiosis expands T helper 17 cells, a key factor in disease exacerbation.
Area of Science:
- Microbiology
- Immunology
- Neuroscience
Background:
- Oral microbiota dysbiosis is linked to multiple sclerosis (MS).
- The precise mechanisms by which oral bacteria influence MS pathogenesis remain unclear.
Purpose of the Study:
- To investigate the role of periodontitis in exacerbating experimental autoimmune encephalomyelitis (EAE), a mouse model of MS.
- To elucidate the underlying mechanisms involving oral pathobionts and T helper 17 (Th17) cell responses.
Main Methods:
- Induction of ligature-induced periodontitis (LIP) in EAE mice.
- Analysis of gut and splenic microbiota composition.
- Flow cytometry to assess Th17 cell populations.
- Fecal microbiota transplantation (FMT) experiments.
Main Results:
- LIP significantly aggravated EAE severity in mice.
- LIP led to an expansion of splenic Th17 cells, associated with increased *Enterobacter* sp.
- Oral pathobionts were enriched in the gut, correlating with increased Th17 cells in the large intestine.
- FMT from LIP-affected EAE mice transmitted disease exacerbation.
Conclusions:
- Periodontitis exacerbates EAE in a mouse model.
- This exacerbation is likely mediated by the expansion of T helper 17 cells.
- Ectopic colonization of oral pathobionts in the gut plays a crucial role in this process.
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