Treatment with Vitamin D/MOG Association Suppresses Experimental Autoimmune Encephalomyelitis
Author(s) -
Fernanda ChiusoMinicucci,
Larissa Lumi Watanabe Ishikawa,
Luiza Ayumi Nishiyama Mimura,
Thais Fernanda de Campos FragaSilva,
Thaís Graziela Donegá França,
Sofia Fernanda Gonçalves Zorzella-Pezavento,
Camila Marques,
Maura Rosane Valério Ikoma,
Alexandrina Sartori
Publication year - 2015
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0125836
Subject(s) - myelin oligodendrocyte glycoprotein , experimental autoimmune encephalomyelitis , multiple sclerosis , encephalomyelitis , immunology , vitamin d and neurology , medicine , spleen , pertussis toxin , receptor , g protein
Experimental autoimmune encephalomyelitis (EAE) is an animal model to study multiple sclerosis (MS). Considering the tolerogenic effects of active vitamin D, we evaluated the therapeutic effect of myelin oligodendrocyte glycoprotein (MOG) associated with active vitamin D in EAE development. EAE was induced in female C57BL/6 mice by immunization with MOG emulsified with Complete Freund’s Adjuvant plus Mycobacterium tuberculosis . Animals also received two intraperitoneal doses of Bordetella pertussis toxin. One day after immunization, mice were treated with 0,1μg of 1α,25-dihydroxyvitamin D3 (1,25(OH) 2 D 3 ) every other day during 15 days (on days 1, 3, 5, 7, 9, 11, 13 and 15). MOG (150μg) was co-administered on days 3 and 11. The administration of 1,25(OH) 2 D 3 or MOG determined significant reduction in EAE incidence and in clinical scores. When MOG was associated with 1,25(OH) 2 D 3 the animals did not develop EAE. Spleen and central nervous system (CNS) cell cultures from this group produced less IL-6 and IL-17 upon stimulation with MOG in comparison to the EAE control group. In addition, this treatment inhibited dendritic cells maturation in the spleen and reduced inflammatory infiltration in the CNS. The association of MOG with 1,25(OH) 2 D 3 was able to control EAE development.
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