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The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases
Multiple sclerosis (MS), neuromyelitis optica (NMO) and myelin oligodendrocyte glycoprotein antibody disease (MOGAD) are inflammatory diseases of the central nervous system (CNS) with a multifactorial aetiology. Environmental factors are important for their development and microorganisms could play...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305018/ https://www.ncbi.nlm.nih.gov/pubmed/37374092 http://dx.doi.org/10.3390/life13061309 |
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author | Frau, Jessica Coghe, Giancarlo Lorefice, Lorena Fenu, Giuseppe Cocco, Eleonora |
author_facet | Frau, Jessica Coghe, Giancarlo Lorefice, Lorena Fenu, Giuseppe Cocco, Eleonora |
author_sort | Frau, Jessica |
collection | PubMed |
description | Multiple sclerosis (MS), neuromyelitis optica (NMO) and myelin oligodendrocyte glycoprotein antibody disease (MOGAD) are inflammatory diseases of the central nervous system (CNS) with a multifactorial aetiology. Environmental factors are important for their development and microorganisms could play a determining role. They can directly damage the CNS, but their interaction with the immune system is even more important. The possible mechanisms involved include molecular mimicry, epitope spreading, bystander activation and the dual cell receptor theory. The role of Epstein–Barr virus (EBV) in MS has been definitely established, since being seropositive is a necessary condition for the onset of MS. EBV interacts with genetic and environmental factors, such as low levels of vitamin D and human endogenous retrovirus (HERV), another microorganism implicated in the disease. Many cases of onset or exacerbation of neuromyelitis optica spectrum disorder (NMOSD) have been described after infection with Mycobacterium tuberculosis, EBV and human immunodeficiency virus; however, no definite association with a virus has been found. A possible role has been suggested for Helicobacter pylori, in particular in individuals with aquaporin 4 antibodies. The onset of MOGAD could occur after an infection, mainly in the monophasic course of the disease. A role for the HERV in MOGAD has been hypothesized. In this review, we examined the current understanding of the involvement of infectious factors in MS, NMO and MOGAD. Our objective was to elucidate the roles of each microorganism in initiating the diseases and influencing their clinical progression. We aimed to discuss both the infectious factors that have a well-established role and those that have yielded conflicting results across various studies. |
format | Online Article Text |
id | pubmed-10305018 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-103050182023-06-29 The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases Frau, Jessica Coghe, Giancarlo Lorefice, Lorena Fenu, Giuseppe Cocco, Eleonora Life (Basel) Review Multiple sclerosis (MS), neuromyelitis optica (NMO) and myelin oligodendrocyte glycoprotein antibody disease (MOGAD) are inflammatory diseases of the central nervous system (CNS) with a multifactorial aetiology. Environmental factors are important for their development and microorganisms could play a determining role. They can directly damage the CNS, but their interaction with the immune system is even more important. The possible mechanisms involved include molecular mimicry, epitope spreading, bystander activation and the dual cell receptor theory. The role of Epstein–Barr virus (EBV) in MS has been definitely established, since being seropositive is a necessary condition for the onset of MS. EBV interacts with genetic and environmental factors, such as low levels of vitamin D and human endogenous retrovirus (HERV), another microorganism implicated in the disease. Many cases of onset or exacerbation of neuromyelitis optica spectrum disorder (NMOSD) have been described after infection with Mycobacterium tuberculosis, EBV and human immunodeficiency virus; however, no definite association with a virus has been found. A possible role has been suggested for Helicobacter pylori, in particular in individuals with aquaporin 4 antibodies. The onset of MOGAD could occur after an infection, mainly in the monophasic course of the disease. A role for the HERV in MOGAD has been hypothesized. In this review, we examined the current understanding of the involvement of infectious factors in MS, NMO and MOGAD. Our objective was to elucidate the roles of each microorganism in initiating the diseases and influencing their clinical progression. We aimed to discuss both the infectious factors that have a well-established role and those that have yielded conflicting results across various studies. MDPI 2023-06-01 /pmc/articles/PMC10305018/ /pubmed/37374092 http://dx.doi.org/10.3390/life13061309 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Frau, Jessica Coghe, Giancarlo Lorefice, Lorena Fenu, Giuseppe Cocco, Eleonora The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases |
title | The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases |
title_full | The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases |
title_fullStr | The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases |
title_full_unstemmed | The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases |
title_short | The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases |
title_sort | role of microorganisms in the etiopathogenesis of demyelinating diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305018/ https://www.ncbi.nlm.nih.gov/pubmed/37374092 http://dx.doi.org/10.3390/life13061309 |
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