Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation

Autor(es)

de Campos Fraga-Silva, Thais Fernanda ^[1] ; Nishiyama Mimura, Luiza Ayumi ^[1] ; Toledo Leite, Laysla de Campos ^[2] ; Borim, Patricia Aparecida ^[3] ; Watanabe Ishikawa, Larissa Lumi ^[1] ; Venturini, James ^[3] ; Parreira de Arruda, Maria Sueli ^[2] ; Sartori, Alexandrina ^[1]

Afiliação do(s) autor(es)

^[1] Sao Paulo State Univ UNESP, Inst Biosci Botucatu, Dept Microbiol & Immunol, BR-18618691 Botucatu, SP - Brazil

^[2] Sao Paulo State Univ UNESP, Sch Sci, Dept Biol Sci, BR-17033360 Bauru, SP - Brazil

^[3] Sao Paulo State Univ UNESP, Botucatu Med Sch, Dept Trop Dis & Image Diag, BR-18618687 Botucatu, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: TOXINS; v. 11, n. 8 AUG 2019.
• Citações Web of Science: 0

Resumo

Gliotoxin (GTX) is the major and the most potent mycotoxin that is secreted by Aspergillus fumigatus, which is capable of injuring and killing microglial cells, astrocytes, and oligodendrocytes. During the last years, studies with patients and experimental models of multiple sclerosis (MS), which is an autoimmune disease of the central nervous system (CNS), suggested that fungal infections are among the possible initiators or aggravators of this pathology. The deleterious effect can occur through a direct interaction of the fungus with the CNS or by the toxin release from a non-neurological site. In the present work, we investigated the effect of GTX on experimental autoimmune encephalomyelitis (EAE) development. Female C57BL/6 mice were immunized with myelin oligodendrocyte glycoprotein and then intraperitoneally injected with three doses of GTX (1 mg/kg b.w., each) on days 4, 7, and 10. GTX aggravated clinical symptoms of the disease in a dose-dependent way and this outcome was concomitant with an increased neuroinflammation. CNS analyses revealed that GTX locally increased the relative expression of inflammatory genes and the cytokine production. Our results indicate that GTX administered in a non-neuronal site was able to increase neuroinflammation in EAE. Other mycotoxins could also be deleterious to many neurological diseases by similar mechanisms. (AU)

• Processo FAPESP: 12/12540-7 - Efeito da infecção com Candida albicans no desenvolvimento da encefalite autoimune experimental
• Beneficiário: Maria Sueli Parreira de Arruda
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 13/14353-2 - Efeito da infecção com Candida albicans no desenvolvimento da Encefalite Autoimune Experimental
• Beneficiário: Thais Fernanda de Campos Fraga da Silva
• Modalidade de apoio: Bolsas no Brasil - Doutorado Direto