SAGE Journals Online
Advertisement
Sign In to gain access to subscriptions and/or personal tools.

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Advertisement

Sign In to gain access to subscriptions and/or personal tools.
Multiple Sclerosis
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
1352458509106856v1
15/10/1135    most recent
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Melanson, M.
Right arrow Articles by Namaka, M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Melanson, M.
Right arrow Articles by Namaka, M.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Experimental autoimmune encephalomyelitis-induced upregulation of tumor necrosis factor-alpha in the dorsal root ganglia

M. Melanson

Faculty of Pharmacy, Apotex Centre, University of Manitoba, Winnipeg, MB, Canada, Department of Neurology Multiple Sclerosis Clinic, Health Sciences Centre, University of Manitoba, Winnipeg, MB, Canada

P. Miao

Faculty of Pharmacy, Apotex Centre, University of Manitoba, Winnipeg, MB, Canada

D. Eisenstat

Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, MB, Canada, Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, MB, Canada, Manitoba Institute of Child Health, University of Manitoba, Winnipeg, MB, Canada

Y. Gong

Faculty of Pharmacy, Apotex Centre, University of Manitoba, Winnipeg, MB, Canada

X. Gu

Faculty of Pharmacy, Apotex Centre, University of Manitoba, Winnipeg, MB, Canada

K. Au

Faculty of Pharmacy, Apotex Centre, University of Manitoba, Winnipeg, MB, Canada, Manitoba Institute of Child Health, University of Manitoba, Winnipeg, MB, Canada

W. Zhu

Faculty of Pharmacy, Apotex Centre, University of Manitoba, Winnipeg, MB, Canada, Manitoba Institute of Child Health, University of Manitoba, Winnipeg, MB, Canada

F. Begum

Manitoba Institute of Child Health, University of Manitoba, Winnipeg, MB, Canada, Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, MB, Canada

EE Frost

Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, MB, Canada, froste{at}cc.umanitoba.ca, Department of Pathology, University of Manitoba, Winnipeg, MB, Canada

M. Namaka

Faculty of Pharmacy, Apotex Centre, University of Manitoba, Winnipeg, MB, Canada, Department of Neurology Multiple Sclerosis Clinic, Health Sciences Centre, University of Manitoba, Winnipeg, MB, Canada, Manitoba Institute of Child Health, University of Manitoba, Winnipeg, MB, Canada

Background: Multiple sclerosis (MS) is a chronic, neurological disease characterized by targeted destruction of central nervous system (CNS) myelin. The autoimmune theory is the most widely accepted explanation of disease pathology. Circulating Th1 cells become activated by exposure to CNS-specific antigens such as myelin basic protein. The activated Th1 cells secrete inflammatory cytokines, which are pivotal for inflammatory responses. We hypothesize that enhanced production of inflammatory cytokines triggers cellular events within the dorsal root ganglia (DRG) and/or spinal cord, facilitating the development of neuropathic pain (NPP) in MS. NPP, the second worst disease-induced symptom suffered by patients with MS, is normally regulated by DRG and/or spinal cord.

Objective: To determine gene and protein expression levels of tumor necrosis factor-alpha (TNF{alpha}) within DRG and/or spinal cord in an animal model of MS.

Methods: Experimental autoimmune encephalomyelitis (EAE) was induced in adolescent female Lewis rats. Animals were sacrificed every 3 days post-disease induction. DRG and spinal cords were harvested for protein and gene expression analysis.

Results: We show significant increases in TNF{alpha} expression in the DRG and of EAE animals at peak disease stage, as assessed by clinical symptoms.

Conclusion: Antigen-induced production of inflammatory cytokines such as TNF{alpha} within the DRG identifies a potential novel mechanism for MS-induced NPP.

Key Words: DRG • EAE • multiple sclerosis • neuropathic pain • tumor necrosis factor-alpha

This version was published on October 1, 2009

Multiple Sclerosis, Vol. 15, No. 10, 1135-1145 (2009)
DOI: 10.1177/1352458509106856


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?




Advertisement