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Brain Advance Access published online on July 10, 2006
Brain, doi:10.1093/brain/awl170
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received February 6, 2006
Revised April 11, 2006
Accepted May 31, 2006

Article

Selective COX-2 inhibitor celecoxib prevents experimental autoimmune encephalomyelitis through COX-2-independent pathway

Katsuichi Miyamoto 1, Sachiko Miyake 2 *, Miho Mizuno 2, Nobuyuki Oka 3, Susumu Kusunoki 4, and Takashi Yamamura 2

1 Department of Immunology, National Institute of Neuroscience, NCNP, Tokyo, Japan; Department of Neurology, Kinki University School of Medicine, Osaka, Japan
2 Department of Immunology, National Institute of Neuroscience, NCNP, Tokyo, Japan
3 Department of Rehabilitation Medicine, Minami-kyoto National Hospital, Kyoto, Japan
4 Department of Neurology, Kinki University School of Medicine, Osaka, Japan

* To whom correspondence should be addressed.
Sachiko Miyake, E-mail: miyake{at}ncnp.go.jp


  Abstract

Cyclooxygenase (COX) is a key enzyme of arachidonic acid metabolism and exists as two distinct isoforms. COX-1 is constitutively expressed in most tissues, whereas COX-2 is inducibly expressed at the site of inflammation. Selective inhibitors of COX-2 have been developed and have been used as anti-inflammatory agents. Here, we show that a new-generation COX-2 inhibitor, celecoxib, inhibited experimental autoimmune encephalomyelitis (EAE). Celecoxib, but not other COX-2 inhibitors such as nimesulid, prevented myelin oligodendrocyte glycoprotein (MOG) induced EAE when administrated orally on the day of disease induction. Moreover, celecoxib inhibited EAE in COX-2-deficient mice, indicating that celecoxib inhibited EAE in a COX-2-independent manner. In celecoxib-treated mice, interferon-{gamma} (IFN-{gamma}) production from MOG-specific T cells was reduced and MOG-specific IgG1 was elevated compared with vehicle-treated mice. Infiltration of inflammatory cells into the central nervous system and the expression of adhesion molecules, P-selectin and intercellular adhesion molecule-1 (ICAM-1), and a chemokine, monocyte chemoattractant peptide-1 (MCP-1), were inhibited when mice were treated with celecoxib. These results suggest that celecoxib may be useful as a new additional therapeutic agent for multiple sclerosis.

Keywords: COX-2 inhibitor; celecoxib; experimental autoimmune encephalomyelitis; multiple sclerosis.
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