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Experimental Autoimmune Encephalomyelitis Development Is Aggravated by Candida albicans Infection
Multiple sclerosis (MS) is an inflammatory/autoimmune disease of the central nervous system (CNS) mainly mediated by myelin specific T cells. It is widely believed that environmental factors, including fungal infections, contribute to disease induction or evolution. Even though Candida infection amo...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4417602/ https://www.ncbi.nlm.nih.gov/pubmed/25969836 http://dx.doi.org/10.1155/2015/635052 |
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author | Fraga-Silva, Thais F. C. Mimura, Luiza A. N. Marchetti, Camila M. Chiuso-Minicucci, Fernanda França, Thais G. D. Zorzella-Pezavento, Sofia F. G. Venturini, James Arruda, Maria S. P. Sartori, Alexandrina |
author_facet | Fraga-Silva, Thais F. C. Mimura, Luiza A. N. Marchetti, Camila M. Chiuso-Minicucci, Fernanda França, Thais G. D. Zorzella-Pezavento, Sofia F. G. Venturini, James Arruda, Maria S. P. Sartori, Alexandrina |
author_sort | Fraga-Silva, Thais F. C. |
collection | PubMed |
description | Multiple sclerosis (MS) is an inflammatory/autoimmune disease of the central nervous system (CNS) mainly mediated by myelin specific T cells. It is widely believed that environmental factors, including fungal infections, contribute to disease induction or evolution. Even though Candida infection among MS patients has been described, the participation of this fungus in this pathology is not clear. The purpose of this work was to evaluate the effect of a Candida albicans infection on experimental autoimmune encephalomyelitis (EAE) that is a widely accepted model to study MS. Female C57BL/6 mice were infected with C. albicans and 3 days later, animals were submitted to EAE induction by immunization with myelin oligodendrocyte glycoprotein. Previous infection increased the clinical score and also the body weight loss. EAE aggravation was associated with expansion of peripheral CD4(+) T cells and production of high levels of TNF-α, IFN-γ IL-6, and IL-17 by spleen and CNS cells. In addition to yeast and hyphae, fungus specific T cells were found in the CNS. These findings suggest that C. albicans infection before EAE induction aggravates EAE, and possibly MS, mainly by CNS dissemination and local induction of encephalitogenic cytokines. Peripheral production of encephalitogenic cytokines could also contribute to disease aggravation. |
format | Online Article Text |
id | pubmed-4417602 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-44176022015-05-12 Experimental Autoimmune Encephalomyelitis Development Is Aggravated by Candida albicans Infection Fraga-Silva, Thais F. C. Mimura, Luiza A. N. Marchetti, Camila M. Chiuso-Minicucci, Fernanda França, Thais G. D. Zorzella-Pezavento, Sofia F. G. Venturini, James Arruda, Maria S. P. Sartori, Alexandrina J Immunol Res Research Article Multiple sclerosis (MS) is an inflammatory/autoimmune disease of the central nervous system (CNS) mainly mediated by myelin specific T cells. It is widely believed that environmental factors, including fungal infections, contribute to disease induction or evolution. Even though Candida infection among MS patients has been described, the participation of this fungus in this pathology is not clear. The purpose of this work was to evaluate the effect of a Candida albicans infection on experimental autoimmune encephalomyelitis (EAE) that is a widely accepted model to study MS. Female C57BL/6 mice were infected with C. albicans and 3 days later, animals were submitted to EAE induction by immunization with myelin oligodendrocyte glycoprotein. Previous infection increased the clinical score and also the body weight loss. EAE aggravation was associated with expansion of peripheral CD4(+) T cells and production of high levels of TNF-α, IFN-γ IL-6, and IL-17 by spleen and CNS cells. In addition to yeast and hyphae, fungus specific T cells were found in the CNS. These findings suggest that C. albicans infection before EAE induction aggravates EAE, and possibly MS, mainly by CNS dissemination and local induction of encephalitogenic cytokines. Peripheral production of encephalitogenic cytokines could also contribute to disease aggravation. Hindawi Publishing Corporation 2015 2015-04-19 /pmc/articles/PMC4417602/ /pubmed/25969836 http://dx.doi.org/10.1155/2015/635052 Text en Copyright © 2015 Thais F. C. Fraga-Silva et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Fraga-Silva, Thais F. C. Mimura, Luiza A. N. Marchetti, Camila M. Chiuso-Minicucci, Fernanda França, Thais G. D. Zorzella-Pezavento, Sofia F. G. Venturini, James Arruda, Maria S. P. Sartori, Alexandrina Experimental Autoimmune Encephalomyelitis Development Is Aggravated by Candida albicans Infection |
title | Experimental Autoimmune Encephalomyelitis Development Is Aggravated by Candida albicans Infection |
title_full | Experimental Autoimmune Encephalomyelitis Development Is Aggravated by Candida albicans Infection |
title_fullStr | Experimental Autoimmune Encephalomyelitis Development Is Aggravated by Candida albicans Infection |
title_full_unstemmed | Experimental Autoimmune Encephalomyelitis Development Is Aggravated by Candida albicans Infection |
title_short | Experimental Autoimmune Encephalomyelitis Development Is Aggravated by Candida albicans Infection |
title_sort | experimental autoimmune encephalomyelitis development is aggravated by candida albicans infection |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4417602/ https://www.ncbi.nlm.nih.gov/pubmed/25969836 http://dx.doi.org/10.1155/2015/635052 |
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