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Mediators of Inflammation
Volume 2016, Article ID 9797021, 10 pages
Research Article

Significant Contribution of Mouse Mast Cell Protease 4 in Early Phases of Experimental Autoimmune Encephalomyelitis

1Department of Pharmacology, Medical School, Université de Sherbrooke, 3001 12th Avenue North, Sherbrooke, QC, Canada J1H 5N4
2Department of Pediatrics, Program of Immunology and Allergology, Medical School, Université de Sherbrooke, 3001 12th Avenue North, Sherbrooke, QC, Canada J1H 5N4
3Department of Medical Biochemistry and Microbiology, Uppsala University BMC, Box 582, 75123 Uppsala, Sweden
4Department of Anatomy, Physiology and Biochemistry, Swedish University of Agricultural Sciences, P.O. Box 7070, 75007 Uppsala, Sweden

Received 20 March 2016; Revised 13 June 2016; Accepted 21 July 2016

Academic Editor: Sandra Helena Penha Oliveira

Copyright © 2016 Louisane Desbiens et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Experimental autoimmune encephalomyelitis (EAE) is a mouse model that reproduces cardinal signs of clinical, histopathological, and immunological features found in Multiple Sclerosis (MS). Mast cells are suggested to be involved in the main inflammatory phases occurring during EAE development, possibly by secreting several autacoids and proteases. Among the latter, the chymase mouse mast cell protease 4 (mMCP-4) can contribute to the inflammatory response by producing endothelin-1 (ET-1). The aim of this study was to determine the impact of mMCP-4 on acute inflammatory stages in EAE. C57BL/6 wild type (WT) or mMCP-4 knockout (KO) mice were immunized with plus complete Freund’s adjuvant followed by pertussis toxin. Immunized WT mice presented an initial acute phase characterized by progressive increases in clinical score, which were significantly reduced in mMCP-4 KO mice. In addition, higher levels of spinal myelin were found in mMCP-4 KO as compared with WT mice. Finally, whereas EAE triggered significant increases in brain levels of mMCP-4 mRNA and immunoreactive ET-1 in WT mice, the latter peptide was reduced to basal levels in mMCP-4 KO congeners. Together, the present study supports a role for mMCP-4 in the early inflammatory phases of the disease in a mouse model of MS.