Oral Pathobionts Promote MS-like Symptoms in Mice

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.