Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 227, Issue 1-2, Pages 133-143Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2010.07.009
Keywords
Laquinimod; Acute axonal damage; Cytokines; EAE; Pathology; VLA-4
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Funding
- University Medical Center Gottingen, Germany
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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. (c) 2010 Elsevier B.V. All rights reserved.
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