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Life
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The Role of Microorganism in the Etiopathogenesis of Demyelinating Diseases
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The Role of Microorganism in the Etiopathogenesis of Demyelinating Diseases

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Microbiology".

Deadline for manuscript submissions: 20 August 2024 | Viewed by 3269

Special Issue Editor

Dr. Davide Cossu

E-Mail Website
Guest Editor
1. Department of Neurology, Juntendo University, Tokyo 113-8421, Japan
2. Department of Biomedical Sciences, Sassari University, 07100 Sassari, Italy
Interests: mycobacteria; multiple sclerosis; EAE; infectious diseases; neuroinflammation

Special Issue Information

Dear Colleagues,

Environmental factors, such as bacterial and viral infections, have been associated with the development of several demyelinating diseases, including multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). However, a direct proof of a causative specific pathogenic agent is still missing.

Moreover, although several studies have demonstrated that several microorganisms may play an important role in the mechanism of the progression of neurological disorders, the underlying mechanisms involved in neuroinflammation, and neuronal degeneration have not been fully clarified.

Since very little is known about the molecular machinery behind the change in the immune system in response to microbial components in patients with demyelinating disorders, this research topic aims to understand the relationship between microorganims, neuroinflammation, and neurodegeneration.

In this Special Issue, we welcome contributions focusing on, but not limited to, the following themes:

  • Role of infection in the etiopathogenesis of MS, NMOSD and MOGAD disorders;
  • Relationship between microbialproducts, immune system and the autoimmune-mediated demyelination;
  • Link between risk of infection reactivation and treatment in demyelinating diseases;
  • Infection in animal model systems of demyelinating diseases

Dr. Davide Cossu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • multiple sclerosis
  • NMOSD
  • MOGAD
  • experimental autoimmune encephalomyelitis (EAE)
  • infection
  • neuroinflammation
  • demyelination

Published Papers (2 papers)

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Research

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12 pages, 1494 KiB  
Article
Mycobacterium avium subsp. paratuberculosis Antigens Elicit a Strong IgG4 Response in Patients with Multiple Sclerosis and Exacerbate Experimental Autoimmune Encephalomyelitis
by Davide Cossu, Yuji Tomizawa, Kazumasa Yokoyama, Tamami Sakanishi, Eiichi Momotani, Leonardo A. Sechi and Nobutaka Hattori
Life 2023, 13(7), 1437; https://doi.org/10.3390/life13071437 - 25 Jun 2023
Cited by 1 | Viewed by 1094
Abstract
Neuroinflammation can be triggered by microbial products disrupting immune regulation. In this study, we investigated the levels of IgG1, IgG2, IgG3, and IgG4 subclasses against the heat shock protein (HSP)70533–545 peptide and lipopentapeptide (MAP_Lp5) derived from Mycobacterium avium subsp. paratuberculosis (MAP) in [...] Read more.
Neuroinflammation can be triggered by microbial products disrupting immune regulation. In this study, we investigated the levels of IgG1, IgG2, IgG3, and IgG4 subclasses against the heat shock protein (HSP)70533–545 peptide and lipopentapeptide (MAP_Lp5) derived from Mycobacterium avium subsp. paratuberculosis (MAP) in the blood samples of Japanese and Italian individuals with relapsing remitting multiple sclerosis (MS). Additionally, we examined the impact of this peptide on MOG-induced experimental autoimmune encephalomyelitis (EAE). A total of 130 Japanese and 130 Italian subjects were retrospectively analyzed using the indirect ELISA method. Furthermore, a group of C57BL/6J mice received immunization with the MAP_HSP70533–545 peptide two weeks prior to the active induction of MOG35–55 EAE. The results revealed a significantly robust antibody response against MAP_HSP70533–545 in serum of both Japanese and Italian MS patients compared to their respective control groups. Moreover, heightened levels of serum IgG4 antibodies specific to MAP antigens were correlated with the severity of the disease. Additionally, EAE mice that were immunized with MAP_HSP70533–545 peptide exhibited more severe disease symptoms and increased reactivity of MOG35–55-specific T-cell compared to untreated mice. These findings provide evidence suggesting a potential link between MAP and the development or exacerbation of MS, particularly in a subgroup of MS patients with elevated serum IgG4 levels. Full article
(This article belongs to the Special Issue The Role of Microorganism in the Etiopathogenesis of Demyelinating Diseases)
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Review

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25 pages, 2015 KiB  
Review
The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases
by Jessica Frau, Giancarlo Coghe, Lorena Lorefice, Giuseppe Fenu and Eleonora Cocco
Life 2023, 13(6), 1309; https://doi.org/10.3390/life13061309 - 01 Jun 2023
Cited by 5 | Viewed by 1705
Abstract
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue The Role of Microorganism in the Etiopathogenesis of Demyelinating Diseases)
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