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Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation
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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6722733/ https://www.ncbi.nlm.nih.gov/pubmed/31357414 http://dx.doi.org/10.3390/toxins11080443 |
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author | Fraga-Silva, Thais Fernanda de Campos Mimura, Luiza Ayumi Nishiyama Leite, Laysla de Campos Toledo Borim, Patrícia Aparecida Ishikawa, Larissa Lumi Watanabe Venturini, James de Arruda, Maria Sueli Parreira Sartori, Alexandrina |
author_facet | Fraga-Silva, Thais Fernanda de Campos Mimura, Luiza Ayumi Nishiyama Leite, Laysla de Campos Toledo Borim, Patrícia Aparecida Ishikawa, Larissa Lumi Watanabe Venturini, James de Arruda, Maria Sueli Parreira Sartori, Alexandrina |
author_sort | Fraga-Silva, Thais Fernanda de Campos |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6722733 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-67227332019-09-10 Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation Fraga-Silva, Thais Fernanda de Campos Mimura, Luiza Ayumi Nishiyama Leite, Laysla de Campos Toledo Borim, Patrícia Aparecida Ishikawa, Larissa Lumi Watanabe Venturini, James de Arruda, Maria Sueli Parreira Sartori, Alexandrina Toxins (Basel) Article 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. MDPI 2019-07-26 /pmc/articles/PMC6722733/ /pubmed/31357414 http://dx.doi.org/10.3390/toxins11080443 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Fraga-Silva, Thais Fernanda de Campos Mimura, Luiza Ayumi Nishiyama Leite, Laysla de Campos Toledo Borim, Patrícia Aparecida Ishikawa, Larissa Lumi Watanabe Venturini, James de Arruda, Maria Sueli Parreira Sartori, Alexandrina Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation |
title | Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation |
title_full | Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation |
title_fullStr | Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation |
title_full_unstemmed | Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation |
title_short | Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation |
title_sort | gliotoxin aggravates experimental autoimmune encephalomyelitis by triggering neuroinflammation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6722733/ https://www.ncbi.nlm.nih.gov/pubmed/31357414 http://dx.doi.org/10.3390/toxins11080443 |
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