Crotoxin down-modulates pro-inflammatory cells and alleviates pain on the MOG35-55-induced experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis

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dc.contributorLaboratório de Dor e Sinalizaçãopt_BR
dc.contributor.authorTeixeira, Nathália Bernardespt_BR
dc.contributor.authorSant'Anna, Morena Brasil Martinspt_BR
dc.contributor.authorGiardini, Aline Carolinapt_BR
dc.contributor.authorAraujo, L.P.pt_BR
dc.contributor.authorFonseca, Lais Aparecidapt_BR
dc.contributor.authorBasso, A.S.pt_BR
dc.contributor.authorCury, Yarapt_BR
dc.contributor.authorPicolo, Giselept_BR
dc.date.accessioned2020-07-09T21:27:00Z-
dc.date.available2020-07-09T21:27:00Z-
dc.date.issued2020pt_BR
dc.identifier.citationTeixeira NB, Sant'Anna MBM, Giardini AC, Araujo L.P., Fonseca LA, Basso A.S., et al. Crotoxin down-modulates pro-inflammatory cells and alleviates pain on the MOG35-55-induced experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Brain. Behav. Immun.. 2020 Feb;84:253-268. doi:10.1016/j.bbi.2019.12.009.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/2982-
dc.description.abstractMultiple sclerosis (MS) is a Central Nervous System inflammatory demyelinating disease that has as primary symptoms losses of sensory and motor functions, including chronic pain. To date, however, few studies have investigated the mechanisms of chronic pain in animal models of MS since locomotor impairments render difficult its evaluation. It was previously demonstrated that in the MOG35-55-induced EAE, an animal model of MS, the hypernociception appears before the onset of motor disability, allowing for the study of these two phenomena separately. Here, we evaluated the effect of crotoxin (CTX), a neurotoxin isolated from the Crotalus durissus terrificus snake venom that displays, at non-toxic dose, antinociceptive, anti-inflammatory and immunomodulatory effects, in the pain and in symptoms progression of EAE. The pain threshold of female C57BL/6 mice decreased at the 4th day after immunization, while the first sign of disease appeared around the 11st–12nd days, coinciding with the onset of motor abnormalities. CTX (40 µg/kg, s.c.) administered in a single dose on the 5th day after immunization, induced a long-lasting analgesic effect (5 days), without interfering with the clinical signs of the disease. On the other hand, when crotoxin was administered for 5 consecutive days, from 5th–9th day after immunization, it induced analgesia and also reduced EAE progression. The antinociceptive effect of crotoxin was blocked by Boc-2 (0.5 mg/kg, i.p.), a selective antagonist of formyl peptide receptors, by NDGA (30 µg/kg, i.p.), a lipoxygenase inhibitor and by atropine sulfate (10 mg/kg, i.p.), an antagonist of muscarinic receptors, administered 30 min before CTX. CTX was also effective in decreasing EAE clinical signs even when administered after its onset. Regarding the interactions between neurons and immunocompetent cells, CTX, in vitro, was able to reduce T cell proliferation, decreasing Th1 and Th17 and increasing Treg cell differentiation. Furthermore, in EAE model, the treatment with 5 consecutive doses of CTX inhibited IFN-?-producing T cells, GM-CSF-producing T cells, reduced the frequency of activated microglia/macrophages within the CNS and decreased the number of migrating cell to spinal cord and cerebellum at the peak of the disease. These results suggest that CTX is a potential treatment not only for pain alteration but also for clinical progression induced by the disease as well as an useful tool for the development of new therapeutic approaches for the multiple sclerosis control.pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)pt_BR
dc.format.extent253-268pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofBrain, Behavior, and Immunitypt_BR
dc.titleCrotoxin down-modulates pro-inflammatory cells and alleviates pain on the MOG35-55-induced experimental autoimmune encephalomyelitis, an animal model of multiple sclerosispt_BR
dc.typeArticlept_BR
dc.identifier.doi10.1016/j.bbi.2019.12.009pt_BR
dc.identifier.urlhttps://doi.org/10.1016/j.bbi.2019.12.009pt_BR
dc.contributor.externalUniversidade Federal de São Paulo (UNIFESP)¦¦Brasilpt_BR
dc.identifier.citationvolume84pt_BR
dc.subject.keywordCrotoxinpt_BR
dc.subject.keywordMultiple sclerosispt_BR
dc.subject.keywordExperimental autoimmune encephalomyelitispt_BR
dc.subject.keywordAnalgesiapt_BR
dc.subject.keywordImmunomodulatory effectpt_BR
dc.relation.ispartofabbreviatedBrain Behav Immunpt_BR
dc.identifier.citationabntv. 84, p. 253-268, fev. 2020pt_BR
dc.identifier.citationvancouver2020 Feb;84:253-268pt_BR
dc.contributor.butantanTeixeira, Nathália Bernardes|:Aluno|:Laboratório de Dor e Sinalização|:PrimeiroAutorpt_BR
dc.contributor.butantanPicolo, Gisele|:Pesquisador:Docente Permanente PPGTOX|:Laboratório de Dor e Sinalização|:Autor de correspondênciapt_BR
dc.contributor.butantanSant'Anna, Morena Brasil Martins|:Aluno|:Laboratório de Dor e Sinalização|:pt_BR
dc.contributor.butantanGiardini, Aline Carolina|:Aluno|:Laboratório de Dor e Sinalização|:pt_BR
dc.contributor.butantanFonseca, Lais Aparecida|:Aluno|:Laboratório de Dor e Sinalização|:pt_BR
dc.contributor.butantanCury, Yara|:Pesquisador|:Laboratório de Dor e Sinalização|:pt_BR
dc.sponsorship.butantanCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)¦¦001pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2010/12903-7pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2011/17974-2pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2013/07467-1pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
item.grantfulltextembargo_29990101-
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