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A polysaccharide from the human commensal Bacteroides fragilis protects against CNS demyelinating disease

J Ochoa-Repáraz1, D W Mielcarz, Y Wang

  • 1Department of Medicine and Neurology, Dartmouth Medical School, Lebanon, New Hampshire, USA. javier.ochoa-reparaz@dartmouth.edu

Mucosal Immunology
|June 10, 2010
PubMed

Insights

Bacteroides fragilis polysaccharide A (PSA) protects against experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS). PSA promotes IL-10 producing regulatory T cells, offering a potential therapeutic strategy for immune-mediated diseases.

Area of Science:

  • Microbiology
  • Immunology
  • Neuroscience

Background:

  • The gut microbiome influences immune-mediated diseases.
  • Gut microflora alterations impact experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS).

Purpose of the Study:

  • To investigate the protective role of polysaccharide A (PSA) from Bacteroides fragilis against EAE.
  • To elucidate the immunomodulatory mechanisms of PSA in EAE.

Main Methods:

  • Oral administration of purified PSA to mice.
  • Analysis of dendritic cell (DC) populations and T cell differentiation.
  • Assessment of EAE development in IL-10-deficient mice.

Main Results:

  • Purified PSA conferred prophylactic and therapeutic protection against EAE.
  • PSA treatment increased CD103+ DCs in cervical lymph nodes.
  • PSA induced the differentiation of naïve CD4+ T cells into IL-10-producing FoxP3+ regulatory T cells (Tregs).
  • Protection was abolished in IL-10-deficient mice.

Conclusions:

  • Bacteroides fragilis PSA protects against EAE.
  • PSA-mediated protection involves the induction of IL-10-producing Tregs.
  • PSA represents a potential therapeutic agent for MS and other immune-mediated diseases.

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