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Cells
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Study around Neuroinflammation—Series 3
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Study around Neuroinflammation—Series 3

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 11606

Special Issue Editor

Prof. Dr. Lars Ove Brandenburg

E-Mail Website
Guest Editor
1. Institute of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany
2. Department of Anatomy and Cell Biology, RWTH Aachen University, 52062 Aachen, Germany
Interests: neuroinflammation; neurodegeneration; bacterial meningitis; antimicrobial peptides; Alzheimer’s disease; multiple sclerosis; glia cells; pattern recognition receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

For some time, it has been known that neuroinflammation is a complex multicellular process that plays a central role in a variety of neurological diseases, including acute inflammation, such as bacterial meningitis, as well as chronic inflammation in form of neurodegenerative diseases or psychiatric and immune-mediated disorders. Numerous findings indicate that neuroinflammation can promote the progression of these disorders. In particular, the function of glial cells (astrocytes and microglial cells), their activation, and also the connection with immigrated immune cells in the disease are of great interest. As a result, there has been an explosion of interest in neuroinflammation and in the tools available to study these processes in the brain.

This Special Issue seeks works covering a wide range of topics related to studies around acute or chronic neuroinflammation, which show the developments of new models or therapeutic approaches or the role of interesting factors or glial cells in various disorders.

The article, on the topic of your choice, can be not only in terms of Reviews but also original Articles, Communication, Hypothesis, Opinion, Perspective, and Systematic Reviews.

Prof. Dr. Lars Ove Brandenburg
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • neuroinflammation
  • neurodegenerative disease
  • bacterial meningitis
  • glia cell
  • microglial cell
  • macrophage
  • astrocyte

Related Special Issues

Published Papers (3 papers)

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Research

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20 pages, 4870 KiB  
Article
T Cell Energy Metabolism Is a Target of Glucocorticoids in Mice, Healthy Humans, and MS Patients
by Leonie Meyer-Heemsoth, Katja Mitschke, Jasmina Bier, Konstantin Schütz, Andreas Villunger, Tobias J. Legler, Martin S. Weber, Fred Lühder and Holger M. Reichardt
Cells 2023, 12(3), 450; https://doi.org/10.3390/cells12030450 - 30 Jan 2023
Cited by 1 | Viewed by 1450
Abstract
Glucocorticoids (GCs) are used to treat inflammatory disorders such as multiple sclerosis (MS) by exerting prominent activities in T cells including apoptosis induction and suppression of cytokine production. However, little is known about their impact on energy metabolism, although it is widely accepted [...] Read more.
Glucocorticoids (GCs) are used to treat inflammatory disorders such as multiple sclerosis (MS) by exerting prominent activities in T cells including apoptosis induction and suppression of cytokine production. However, little is known about their impact on energy metabolism, although it is widely accepted that this process is a critical rheostat of T cell activity. We thus tested the hypothesis that GCs control genes and processes involved in nutrient transport and glycolysis. Our experiments revealed that escalating doses of dexamethasone (Dex) repressed energy metabolism in murine and human primary T cells. This effect was mediated by the GC receptor and unrelated to both apoptosis induction and Stat1 activity. In contrast, treatment of human T cells with rapamycin abolished the repression of metabolic gene expression by Dex, unveiling mTOR as a critical target of GC action. A similar phenomenon was observed in MS patients after intravenous methylprednisolon (IVMP) pulse therapy. The expression of metabolic genes was reduced in the peripheral blood T cells of most patients 24 h after GC treatment, an effect that correlated with disease activity. Collectively, our results establish the regulation of T cell energy metabolism by GCs as a new immunomodulatory principle. Full article
(This article belongs to the Special Issue Study around Neuroinflammation—Series 3)
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Review

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30 pages, 1374 KiB  
Review
Microglia Mediated Neuroinflammation in Parkinson’s Disease
by Sevim Isik, Bercem Yeman Kiyak, Rumeysa Akbayir, Rama Seyhali and Tahire Arpaci
Cells 2023, 12(7), 1012; https://doi.org/10.3390/cells12071012 - 25 Mar 2023
Cited by 22 | Viewed by 6369
Abstract
Parkinson’s Disease (PD) is the second most common neurodegenerative disorder seen, especially in the elderly. Tremor, shaking, movement problems, and difficulty with balance and coordination are among the hallmarks, and dopaminergic neuronal loss in substantia nigra pars compacta of the brain and aggregation [...] Read more.
Parkinson’s Disease (PD) is the second most common neurodegenerative disorder seen, especially in the elderly. Tremor, shaking, movement problems, and difficulty with balance and coordination are among the hallmarks, and dopaminergic neuronal loss in substantia nigra pars compacta of the brain and aggregation of intracellular protein α-synuclein are the pathological characterizations. Neuroinflammation has emerged as an involving mechanism at the initiation and development of PD. It is a complex network of interactions comprising immune and non-immune cells in addition to mediators of the immune response. Microglia, the resident macrophages in the CNS, take on the leading role in regulating neuroinflammation and maintaining homeostasis. Under normal physiological conditions, they exist as “homeostatic” but upon pathological stimuli, they switch to the “reactive state”. Pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes are used to classify microglial activity with each phenotype having its own markers and released mediators. When M1 microglia are persistent, they will contribute to various inflammatory diseases, including neurodegenerative diseases, such as PD. In this review, we focus on the role of microglia mediated neuroinflammation in PD and also signaling pathways, receptors, and mediators involved in the process, presenting the studies that associate microglia-mediated inflammation with PD. A better understanding of this complex network and interactions is important in seeking new therapies for PD and possibly other neurodegenerative diseases. Full article
(This article belongs to the Special Issue Study around Neuroinflammation—Series 3)
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28 pages, 3667 KiB  
Review
COVID-19 and Multiple Sclerosis: A Complex Relationship Possibly Aggravated by Low Vitamin D Levels
by William Danilo Fernandes de Souza, Denise Morais da Fonseca and Alexandrina Sartori
Cells 2023, 12(5), 684; https://doi.org/10.3390/cells12050684 - 21 Feb 2023
Cited by 3 | Viewed by 3374
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an exceptionally transmissible and pathogenic coronavirus that appeared at the end of 2019 and triggered a pandemic of acute respiratory disease, known as coronavirus disease 2019 (COVID-19). COVID-19 can evolve into a severe disease associated [...] Read more.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an exceptionally transmissible and pathogenic coronavirus that appeared at the end of 2019 and triggered a pandemic of acute respiratory disease, known as coronavirus disease 2019 (COVID-19). COVID-19 can evolve into a severe disease associated with immediate and delayed sequelae in different organs, including the central nervous system (CNS). A topic that deserves attention in this context is the complex relationship between SARS-CoV-2 infection and multiple sclerosis (MS). Here, we initially described the clinical and immunopathogenic characteristics of these two illnesses, accentuating the fact that COVID-19 can, in defined patients, reach the CNS, the target tissue of the MS autoimmune process. The well-known contribution of viral agents such as the Epstein-Barr virus and the postulated participation of SARS-CoV-2 as a risk factor for the triggering or worsening of MS are then described. We emphasize the contribution of vitamin D in this scenario, considering its relevance in the susceptibility, severity and control of both pathologies. Finally, we discuss the experimental animal models that could be explored to better understand the complex interplay of these two diseases, including the possible use of vitamin D as an adjunct immunomodulator to treat them. Full article
(This article belongs to the Special Issue Study around Neuroinflammation—Series 3)
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