Immunomodulation of experimental allergic encephalomyelitis by cinnamon metabolite sodium benzoate

• Published in: Immunopharmacology and immunotoxicology Vol. 33; no. 4; pp. 586 - 593
• Main Author: Pahan, Kalipada
• Format: Journal Article
• Language: English
• Published: England Informa Healthcare 01.12.2011; Taylor & Francis
• Subjects: adaptive immunity; Animal models; Animals; Cell activation; Cell Communication - drug effects; Cell migration; Cell Movement - drug effects; Cell Movement - immunology; Central nervous system; Children; cinnamon; Demyelinating diseases; Drugs; EAE; Encephalomyelitis, Autoimmune, Experimental - drug therapy; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - pathology; Experimental allergic encephalomyelitis; Food additives; Food Preservatives - therapeutic use; glial activation; Glial cells; Humans; Immune response; Immunologic Factors - therapeutic use; Immunomodulation; Immunoregulation; Immunosuppressive agents; Inflammation; Inflammation - drug therapy; Inflammation - immunology; Inflammation - pathology; Inflammatory diseases; innate immunity; Lymphocytes T; Metabolites; Mice; microbicides; Multiple sclerosis; Multiple Sclerosis - drug therapy; Multiple Sclerosis - immunology; Multiple Sclerosis - pathology; Neuroglia - immunology; Neuroglia - pathology; Neuroimmunology; neuroinflammation; Signal transduction; Signal Transduction - drug effects; Signal Transduction - immunology; Sodium benzoate; Sodium Benzoate - therapeutic use; T-Lymphocytes, Helper-Inducer - immunology; T-Lymphocytes, Helper-Inducer - pathology; Urea
• ISSN: 0892-3973; 1532-2513
• DOI: 10.3109/08923973.2011.561861

Experimental allergic encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS), the most common human demyelinating disease of the central nervous system. Sodium benzoate (NaB), a metabolite of cinnamon and a FDA-approved drug against urea cycle disorders in children, is a widely used food additive, which is long known for its microbicidal effect. However, recent studies reveal that apart from its microbicidal effects, NaB can also regulate many immune signaling pathways responsible for inflammation, glial cell activation, switching of T-helper cells, modulation of regulatory T cells, cell-to-cell contact, and migration. As a result, NaB alters the neuroimmunology of EAE and ameliorates the disease process of EAE. In this review, we have made an honest attempt to analyze these newly-discovered immunomodulatory activities of NaB and associated mechanisms that may help in considering this drug for various inflammatory human disorders including MS as primary or adjunct therapy.