Protective mechanisms by omega-6 lipids in experimental autoimmune encephalomyelitis (EAE) are associated with cytokines and eicosanoids
| Autor: | Laurence S. Harbige, Margaret M Morris, Sandra Amor, Lorna Layward |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
medicine.medical_specialty
Proteolipid protein 1 Encephalomyelitis Autoimmune Experimental Lymphocyte Encephalomyelitis T-Lymphocytes Administration Oral Mice Inbred Strains Lymphocyte Activation Biochemistry Dinoprostone Myelin oligodendrocyte glycoprotein Mice Immune system Dietary Fats Unsaturated immune system diseases Transforming Growth Factor beta Internal medicine Fatty Acids Omega-6 medicine Demyelinating disease Animals Plant Oils gamma-Linolenic Acid Cells Cultured biology Chemistry Experimental autoimmune encephalomyelitis Plants medicine.disease nervous system diseases Myelin basic protein medicine.anatomical_structure Endocrinology biology.protein Fatty Acids Unsaturated |
| Zdroj: | Biochemical Society transactions. 25(2) |
| ISSN: | 0300-5127 |
| Popis: | Experimental autoimmune encephalomyelitis (EAE) is an autoimmune and demyelinating disease of the central nervous system (CNS) inducible in susceptible rodents and other mammalian species by active or adoptive sensitization to CNS constituents [I]. EAE can be induced by inoculation with neuroantigens such as myelin basic protein (MBP), proteolipid protein (PLP), myelin oligodendrocyte glycoprotein (MOG) and their peptides [ 1-31. We have reported previously that oral administration of lipid, rich in the omega-6 fatty acid ylinolenic acid, can completely protect Lewis rats from spinal cord homogenate induced EAE [4]. In contrast we have found that omega-3 fatty acids exacerbate and prolong EAE in Lewis rats [5,6]. The mechanisms by which y-linolenic acid modifies the immune response in EAE is unclear. We have, therefore, investigated the effects of oral feeding a y-linolenic acid-rich plant lipid (Borago offcinalis) on MOG-peptide (aa 92-106) induced EAE in SJL mice. Lymphocyte proliferative responses and the production of cytokines and eicosanoids ex vivo were also investigated. MOG-peptide (aa 92-106) induced EAE, in SJL mice, was carried out as described previously [3]. Mice were galvaged daily with 250-300 1.11 plant lipid (B. oficinalis) from day 7 after EAE induction and sacrificed at day 21. Mice were examined daily and clinical signs assessed. Brain and spinal cord were processed for routine histology [3]. Mononuclear cells were isolated from spleens by density centrifugation and cultured for 72 hr with ConA (lpg/ml), PPD (1:lO) and MOG peptide (aa 92-106; 5pg/ml). Proliferation was assessed by 3H thymidine incorporation. Culture supernatants, 24 hr, were assayed for IL-2, IFNy and IL-4 using ELISA (Genzyme, USA) and TGFfi, measured by a modified TGFP, ELISA system (Promega, USA). PGE, was assayed by competitive immunoassay (Cayman USA). The clinical and histological manifestations of EAE in SJL mice were markedly inhibited by lipid feeding (Table 1). |
| Databáze: | OpenAIRE |
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