Pro-inflammatory influence of high sucrose consumption on experimental autoimmune encephalomyelitis mouse immunized with MOG35-55

Abstract

Experimental autoimmune encephalomyelitis (EAE) is the most often used animal model for the multiple sclerosis (MS). EAE is characterized by the complex symptoms of neuropathology and immunopathology leading to similar key symptoms of MS. In this study, we evaluated the influence of high sucrose (HS) consumption in the autoimmune disease pathogenesis. In brief, 7- 8 weeks old C57BL/6J mice were randomly distributed into three following groups for 30 days: healthy control, EAE, and EAE+HS (20 % sucrose in a drink). To establish an EAE mouse model, all mice except those in healthy control were sensitized with MOG35-55. The EAE in HS-induced mice was worsened as shown by higher clinical scores, infiltrated inflammatory cells, severe demyelination, making disease at the peak in brain and spinal cord compared to healthy control. Additionally, the chronic exposure of HS exhibited excessive lipid accumulation in the liver. Furthermore, mRNA expressions of TGF-β, IL-17A, and MCP-1 in central nervous system (CNS) were significantly higher in EAE+HS compared to EAE or healthy control. EAE+HS group also showed the exacerbation of inflammatory gene expressions, i.e., IFN-γ, TNF-α, IL-1β, IL-6, and IL-22 for the differentiation of Th1 and Th17 cells. Conclusively, the results indicate high sucrose consumption promotes axonal damage, inflammation, and demyelination in EAE mice. Key words; Experimental autoimmune encephalomyelitis, Multiple sclerosis, High sucrose, Central nervous system