Journal article
Diminished cytokine and chemokine expression in the central nervous system of GMF-deficient mice with experimental autoimmune encephalomyelitis
Brain research, Vol.1144(1), pp.239-247
2007
DOI: 10.1016/j.brainres.2007.01.075
PMCID: PMC1899479
PMID: 17316572
Abstract
Pro-inflammatory cytokines/chemokines are implemented in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model with clinical and pathological similarities to multiple sclerosis. We have previously shown that over-expression of glia maturation factor (GMF) in glial cells cause excessive production and secretion of pro-inflammatory cytokines/chemokines sufficient to destroy the myelin-forming oligodendroglial cell
in vitro. In this present investigation, we evaluate the expression of pro-inflammatory mediators in the central nervous system (CNS) of GMF+/+ (wild type) mice and GMF−/− (GMF-knockout) mice at the peak of EAE induced by immunization with MOG 35–55 peptide. GMF+/+ (Wt) mice developed severe EAE with a maximal mean clinical score of 3.6
±
0.5 by day 16 post-immunization, whereas GMF-KO mice showed significantly delayed EAE with an average onset on day 26 pi with reduced mean clinical score of 1.3
±
0.3. Three of fifteen Wt mice as compared to none of GMF-KO mice died of EAE. Encephalitogenic cells from Wt mice transferred to recipient GMF-KO mice caused very mild and with low incidence of EAE. We determined the differences in the expression of cytokines, IFN-γ, TNF-α, IL-1 β, IL-6, IL-4, IL-10, and chemokines, MIP-1, MIP-2, IP-10, MCP-1, GM-CSF mRNA by quantitative real-time RT–PCR in brain and spinal cord. Our results demonstrate significantly low levels of pro-inflammatory cytokines/chemokines in the CNS of GMF-KO mice and increased expression in Wt mice with EAE. Our data suggest that GMF play a critical role in CNS inflammation.
Details
- Title: Subtitle
- Diminished cytokine and chemokine expression in the central nervous system of GMF-deficient mice with experimental autoimmune encephalomyelitis
- Creators
- Asgar Zaheer - University of Iowa, NeurologyShailendra K Sahu - Division of Neurochemistry and Neurobiology, Department of Neurology, The University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242, USAYanghong Wu - Division of Neurochemistry and Neurobiology, Department of Neurology, The University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242, USAAshna Zaheer - Department of Obstetric and Gynecology, University of Iowa, Iowa City, IA 52242, USAJoel Haas - Veterans Affair Medical Center, Iowa City, IA 52242, USAKiwhoon Lee - Division of Neurochemistry and Neurobiology, Department of Neurology, The University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242, USABaoli Yang - University of Iowa, BioVentures Center
- Resource Type
- Journal article
- Publication Details
- Brain research, Vol.1144(1), pp.239-247
- DOI
- 10.1016/j.brainres.2007.01.075
- PMID
- 17316572
- PMCID
- PMC1899479
- NLM abbreviation
- Brain Res
- ISSN
- 0006-8993
- eISSN
- 1872-6240
- Publisher
- Elsevier B.V
- Language
- English
- Date published
- 2007
- Academic Unit
- Neurology; BioVentures Center; Obstetrics and Gynecology
- Record Identifier
- 9983557773602771
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