HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Brahmachari, S. Articles by Pahan, K. Search for Related Content PubMed PubMed Citation Articles by Brahmachari, S. Articles by Pahan, K.

Sodium Benzoate, a Food Additive and a Metabolite of Cinnamon, Modifies T Cells at Multiple Steps and Inhibits Adoptive Transfer of Experimental Allergic Encephalomyelitis¹

Saurav Brahmachari^* and Kalipada Pahan^2,*,

^* Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612; and Department of Oral Biology, Section of Neuroscience, University of Nebraska Medical Center College of Dentistry, Lincoln, NE 68583

Experimental allergic encephalomyelitis (EAE) is the animal model for multiple sclerosis. This study explores a novel use of sodium benzoate (NaB), a commonly used food additive and a Food and Drug Administration-approved nontoxic drug for urea cycle disorders, in treating the disease process of relapsing-remitting EAE in female SJL/J mice. NaB, administered through drinking water at physiologically tolerable doses, ameliorated clinical symptoms and disease progression of EAE in recipient mice and suppressed the generation of encephalitogenic T cells in donor mice. Histological studies reveal that NaB effectively inhibited infiltration of mononuclear cells and demyelination in the spinal cord of EAE mice. Consequently, NaB also suppressed the expression of proinflammatory molecules and normalized myelin gene expression in the CNS of EAE mice. Furthermore, we observed that NaB switched the differentiation of myelin basic protein-primed T cells from Th1 to Th2 mode, enriched regulatory T cell population, and down-regulated the expression of various contact molecules in T cells. Taken together, our results suggest that NaB modifies encephalitogenic T cells at multiple steps and that NaB may have therapeutic importance in multiple sclerosis.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This study was supported by grants from the National Multiple Sclerosis Society (RG3422A1/1) and National Institutes of Health (NS39940 and NS48923).

² Address correspondence and reprint requests to Dr. Kalipada Pahan, Department of Neurological Sciences, Rush University Medical Center, 1735 West Harrison Street, Suite 320, Chicago, IL 60612. E-mail address: Kalipada_Pahan{at}rush.edu

³ Abbreviations used in this paper: MS, multiple sclerosis; Tregs, regulatory T cell; EAE, experimental allergic encephalomyelitis; NaB, sodium benzoate; RR-EAE, relapsing-remitting model of EAE; NaFO, sodium formate; dpt, days posttransfer; BBB, blood-brain barrier; MOG, myelin oligodendrocyte glycoprotein; iNOS, inducible NO synthase; PLP, proteolipid protein; CNPase, 2',3'-cyclic nucleotide 3-phosphodiesterase.