Ribavirin ameliorates experimental autoimmune encephalomyelitis in rats and modulates cytokine production
| Autor: | Sanja Dacic, Danijela Stojkov, Sanja Pekovic, Ljubisav Rakic, Stanislava Stosic-Grujicic, Irena Lavrnja, Ivana Bjelobaba, Marija Mostarica-Stojkovic, Nadezda Nedeljkovic, Mirjana Stojiljkovic |
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| Jazyk: | angličtina |
| Rok vydání: | 2008 |
| Předmět: |
Central Nervous System
Encephalomyelitis Autoimmune Experimental medicine.medical_treatment Encephalomyelitis Immunology Central nervous system Biology medicine.disease_cause Antiviral Agents Autoimmunity 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Ribavirin medicine Immunology and Allergy Animals Cells Cultured 030304 developmental biology Pharmacology 0303 health sciences Multiple sclerosis Experimental autoimmune encephalomyelitis virus diseases Brain medicine.disease Immunohistochemistry 3. Good health Rats Cytokine medicine.anatomical_structure chemistry Spinal Cord Experimental pathology Cytokines Female Lymph Nodes 030217 neurology & neurosurgery |
| Zdroj: | International Immunopharmacology |
| Popis: | To determine the mechanism underlying ribavirin induced amelioration of experimental autoimmune encephalomyelitis (EAE), cytokine profiles were evaluated in draining lymph node (DLN) cell culture supernatants and spinal cord obtained from EAE and/or ribavirin-treated EAE Dark Agouti rats. Administration of ribavirin to EAE rats markedly affected the production of pro-inflammatory cytokines IFN-gamma, IL-1 beta and TNF-alpha in DLN and spinal cord, thus shifting the balance towards the anti-inflammatory cytokines IL-10 and TGF-beta. These findings suggest that ribavirin attenuates EAE by limiting cytokine-mediated immunoinflammatory events leading to CNS destruction. The conducted experiments provide rationale for ribavirin to be considered as a candidate drug in the development of new therapeutic strategies for the treatment of autoimmune diseases in humans, such as multiple sclerosis. (c) 2008 Elsevier B.V. All rights reserved. null |
| Databáze: | OpenAIRE |
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