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Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
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Thiamine deficiency promotes T cell infiltration in experimental autoimmune encephalomyelitis: the involvement of

Zhe Ji1, Zhiqin Fan1, Ying Zhang2

  • 1Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China;

Journal of Immunology (Baltimore, Md. : 1950)
|July 27, 2014
PubMed

Insights

Thiamine deficiency (TD) worsens experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. TD increases inflammation and immune cell infiltration by upregulating CCL2, exacerbating EAE pathogenesis.

Area of Science:

  • Neuroimmunology
  • Autoimmune Diseases
  • Nutritional Neuroscience

Background:

  • Multiple sclerosis (MS) is a complex neurological disorder influenced by genetic and environmental factors.
  • Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model to study MS pathogenesis.
  • Chemokines like CCL2 play a role in EAE development, and thiamine deficiency (TD) has been shown to induce CCL2.

Purpose of the Study:

  • To investigate the hypothesis that thiamine deficiency (TD) affects the pathogenesis of experimental autoimmune encephalomyelitis (EAE).
  • To determine the impact of TD on clinical and pathological outcomes in an EAE mouse model.

Main Methods:

  • EAE was induced in C57BL/6J mice using myelin oligodendroglial glycoprotein (MOG) peptides 35-55, with or without concurrent thiamine deficiency (TD).
  • Clinical scores and spinal cord pathology were assessed.
  • An adoptive transfer EAE model was used to evaluate TD's effect on disease progression. Immune cell infiltration, T cell subtypes (Th1, Th17), CCL2, and CCR2 expression were analyzed. In vitro assays assessed T lymphocyte proliferation and migration stimulated by CCL2.

Main Results:

  • Thiamine deficiency (TD) significantly aggravated EAE development, evidenced by increased clinical scores and spinal cord pathology.
  • TD accelerated EAE progression in an adoptive transfer model and led to microglial activation and a 140% increase in leukocyte infiltration in the spinal cord.
  • TD elevated Th1 and Th17 cell populations and upregulated CCL2 and CCR2 expression in the spinal cord. MOG-primed TD lymphocytes showed enhanced proliferation, and CCL2 stimulated T lymphocyte proliferation and migration in vitro.

Conclusions:

  • Thiamine deficiency exacerbates experimental autoimmune encephalomyelitis (EAE) by promoting neuroinflammation.
  • The exacerbation is linked to increased CCL2 expression and subsequent enhanced leukocyte infiltration, particularly Th1 and Th17 cells.
  • TD negatively impacts T cell responses, contributing to the heightened severity of EAE.

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