Oral chitin treatment improved demyelination in murine autoimmune encephalomyelitis model by inhibition of inflammatory responses

Int Immunopharmacol. 2020 Jul:84:106536. doi: 10.1016/j.intimp.2020.106536. Epub 2020 Apr 30.


This study aimed to determine whether chitin microparticles (CMP), glucosamine-based polymers, have an anti-inflammatory response in a murine model of autoimmune encephalomyelitis. Experimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice by immunization with myelin antigens emulsified in complete Freund adjuvant. A standard clinical and histological method (Luxol Fast Blue staining) was used to validate the model and document the impact of CMP treatment. ELISA was used to determine the production of spleen cell cytokines and serum levels of anti-chitin antibodies. Flowcytometry was used to determine the percentage of regulatory lymphocytes. The relative expression of the breast regression protein 39 (BRP-39) gene was examined through real time-PCR amplification. Clinical signs were significantly improved in mice given CMP compared with untreated mice. Histological analysis of the spinal cord revealed that treatment significantly reduced demyelination. The levels of interferon-γ, interleukin-17, and tumor necrosis factor-α were also reduced; conversely, no significant change was detected in interleukin-10 level and regulatory T cell count. The CMP-fed mice showed lower BRP-39 expression compared with the control group. It was ultimately determined that CMP modulates immune responses which could indirectly alter the pathology of an injured central nervous system. The data suggests that CMP may be used as an effective and cheap oral therapeutic agent for multiple sclerosis.

Keywords: Chitin; Chitinase; Experimental Autoimmune Encephalomyelitis (EAE); Multiple sclerosis.

MeSH terms

  • Administration, Oral
  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Anti-Inflammatory Agents / therapeutic use*
  • Brain / drug effects
  • Brain / metabolism
  • Chitin / pharmacology
  • Chitin / therapeutic use*
  • Chitinase-3-Like Protein 1 / genetics
  • Cytokines / immunology
  • Encephalomyelitis, Autoimmune, Experimental / drug therapy*
  • Encephalomyelitis, Autoimmune, Experimental / genetics
  • Encephalomyelitis, Autoimmune, Experimental / immunology
  • Encephalomyelitis, Autoimmune, Experimental / pathology
  • Female
  • Gene Expression Regulation / drug effects
  • Immunoglobulin G / blood
  • Immunologic Factors / pharmacology
  • Immunologic Factors / therapeutic use*
  • Mice, Inbred C57BL
  • Multiple Sclerosis / drug therapy
  • Spinal Cord / drug effects
  • Spinal Cord / pathology
  • Spleen / cytology
  • Spleen / immunology
  • T-Lymphocytes, Regulatory / drug effects
  • T-Lymphocytes, Regulatory / immunology


  • Anti-Inflammatory Agents
  • Chil1 protein, mouse
  • Chitinase-3-Like Protein 1
  • Cytokines
  • Immunoglobulin G
  • Immunologic Factors
  • Chitin