Abstract |
We investigated the effect of laquinimod on inflammatory demyelination, axonal damage, cytokine profiles and migratory capacities of lymphocytes in C57BL/6 mice with active EAE induced with MOG(35-55) peptide. The mice were treated at disease induction and after disease onset. Spinal cords were assessed histologically. Cytokines and adhesive properties were analyzed in splenocytes. Preventive and therapeutic laquinimod treatment reduced clinical signs, inflammation, and demyelination. VLA-4-mediated adhesiveness and pro-inflammatory cytokines such as IL-17 were down-regulated in treated animals. Within lesions, treated mice showed similar axonal densities, but less acute axonal damage than controls. Laquinimod might thus protect myelin and axons by decreasing pro-inflammatory cytokines and impairing the migratory capacity of lymphocytes.
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Authors | Christiane Wegner, Christine Stadelmann, Ramona Pförtner, Emanuel Raymond, Sara Feigelson, Ronen Alon, Bracha Timan, Liat Hayardeny, Wolfgang Brück |
Journal | Journal of neuroimmunology
(J Neuroimmunol)
Vol. 227
Issue 1-2
Pg. 133-43
(Oct 08 2010)
ISSN: 1872-8421 [Electronic] Netherlands |
PMID | 20684995
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2010 Elsevier B.V. All rights reserved. |
Chemical References |
- Inflammation Mediators
- Interleukin-17
- Quinolones
- laquinimod
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Topics |
- Animals
- Axons
(drug effects, immunology, pathology)
- Cell Movement
(drug effects, immunology)
- Demyelinating Diseases
(drug therapy, immunology, pathology)
- Down-Regulation
(drug effects, immunology)
- Encephalomyelitis, Autoimmune, Experimental
(drug therapy, immunology, pathology)
- Female
- Inflammation Mediators
(therapeutic use)
- Interleukin-17
(antagonists & inhibitors, metabolism)
- Mice
- Mice, Inbred C57BL
- Quinolones
(therapeutic use)
- T-Lymphocyte Subsets
(drug effects, immunology, pathology)
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