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Microglia: On the Cutting Edge between Health and Disease
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Microglia: On the Cutting Edge between Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 October 2020) | Viewed by 19590

Special Issue Editors

Prof. Dr. Cordian Beyer

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Guest Editor
Rheinisch-Westfalische Technische Hochschule Aachen, Institute of Neuroanatomy, Aachen, Germany
Interests: neurodegenerative diseases; CNS; neuroinflammatory processes
Prof. Dr. Markus Kipp

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Co-Guest Editor
Department of Anatomy, Rostock University Medical Center, 18055 Rostock, Germany
Interests: neurobiology; neuroscience; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Microglia derive from the yolk sac, colonize at an early developmental stage the CNS, and function there as resident innate immune cells. Microglia is continually surveying the microenvironment with their motile branches, activated by different stimuli, and embedded in local immune responses including phagocytosis and antigen presentation. Microglial cells show rapid chemotactic reactions to damage, switch from a protective to a destructive cell type and vice versa, and form a regulatory immune network with astroglia. These features have relevance for neurodegenerative diseases and CNS trauma where reactive microglia plays an etiological role. During development and lifelong, microglia have a seminal role in proper synapse formation by eliminating or strengthen synaptic contacts, thereby continuously reorganizing and fine-tuning neural networks. Based on this broad spectrum of microglia, we interpret them as immune cell type with remarkable plasticity and a wide range of tasks. Environmental and social stressors associated with depression and pain also target microglia and trigger neuroinflammation at different amplitudes. Thus, microglia represents the cellular interface to modulate depression-related and pain neural circuits. The understanding of the high measure of flexibility and adaptability of microglia in the healthy and injured CNS could offer better diagnostic and therapeutic approaches for neurological disorders.

Prof. Cordian Beyer
Prof. Markus Kipp
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Published Papers (5 papers)

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Research

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17 pages, 4328 KiB  
Article
Sex-Specific Effects of Microglia-Like Cell Engraftment during Experimental Autoimmune Encephalomyelitis
by Jinming Han, Keying Zhu, Kai Zhou, Ramil Hakim, Sreenivasa Raghavan Sankavaram, Klas Blomgren, Harald Lund, Xing-Mei Zhang and Robert A. Harris
Int. J. Mol. Sci. 2020, 21(18), 6824; https://doi.org/10.3390/ijms21186824 - 17 Sep 2020
Cited by 12 | Viewed by 2988
Abstract
Multiple sclerosis (MS) is a chronic neuroinflammatory disorder of the central nervous system (CNS) that usually presents in young adults and predominantly in females. Microglia, a major resident immune cell in the CNS, are critical players in both CNS homeostasis and disease. We [...] Read more.
Multiple sclerosis (MS) is a chronic neuroinflammatory disorder of the central nervous system (CNS) that usually presents in young adults and predominantly in females. Microglia, a major resident immune cell in the CNS, are critical players in both CNS homeostasis and disease. We have previously demonstrated that microglia can be efficiently depleted by the administration of tamoxifen in Cx3cr1CreER/+Rosa26DTA/+ mice, with ensuing repopulation deriving from both the proliferation of residual CNS resident microglia and the engraftment of peripheral monocyte-derived microglia-like cells. In this study, tamoxifen was administered to Cx3cr1CreER/+Rosa26DTA/+ and Cx3cr1CreER/+ female and male mice. Experimental autoimmune encephalomyelitis (EAE), a widely used animal model of MS, was induced by active immunization with myelin oligodendrocyte glycoprotein (MOG) one month after tamoxifen injections in Cx3cr1CreER/+Rosa26DTA/+ mice and Cx3cr1CreER/+ mice, a time point when the CNS niche was colonized by microglia derived from both CNS microglia and peripherally-derived macrophages. We demonstrate that engraftment of microglia-like cells following microglial depletion exacerbated EAE in Cx3cr1CreER/+Rosa26DTA/+ female mice as assessed by clinical symptoms and the expression of CNS inflammatory factors, but these findings were not evident in male mice. Higher major histocompatibility complex class II expression and cytokine production in the female CNS contributed to the sex-dependent EAE severity in mice following engraftment of microglia-like cells. An underestimated yet marked sex-dependent microglial activation pattern may exist in the injured CNS during EAE. Full article
(This article belongs to the Special Issue Microglia: On the Cutting Edge between Health and Disease)
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12 pages, 1395 KiB  
Article
Exosomal MiRNA Transfer between Retinal Microglia and RPE
by Dorothea R. Morris, Sarah E. Bounds, Huanhuan Liu, Wei-Qun Ding, Yan Chen, Yin Liu and Jiyang Cai
Int. J. Mol. Sci. 2020, 21(10), 3541; https://doi.org/10.3390/ijms21103541 - 17 May 2020
Cited by 33 | Viewed by 3805
Abstract
The retinal pigment epithelium (RPE), the outermost layer of the retina, provides essential support to both the neural retina and choroid. Additionally, the RPE is highly active in modulating functions of immune cells such as microglia, which migrate to the subretinal compartment during [...] Read more.
The retinal pigment epithelium (RPE), the outermost layer of the retina, provides essential support to both the neural retina and choroid. Additionally, the RPE is highly active in modulating functions of immune cells such as microglia, which migrate to the subretinal compartment during aging and age-related degeneration. Recently, studies have highlighted the important roles of microRNA (miRNA) in the coordination of general tissue maintenance as well as in chronic inflammatory conditions. In this study, we analyzed the miRNA profiles in extracellular vesicles (EVs) released by the RPE, and identified and validated miRNA species whose expression levels showed age-dependent changes in the EVs. Using co-culture of RPE and retinal microglia, we further demonstrated that miR-21 was transferred between the two types of cells, and the increased miR-21 in microglia influenced the expression of genes downstream of the p53 pathway. These findings suggest that exosome-mediated miRNA transfer is a signaling mechanism that contributes to the regulation of microglia function in the aging retina. Full article
(This article belongs to the Special Issue Microglia: On the Cutting Edge between Health and Disease)
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Review

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18 pages, 1756 KiB  
Review
New Insights into Immune-Mediated Mechanisms in Parkinson’s Disease
by Jolene Su Yi Tan, Yin Xia Chao, Olaf Rötzschke and Eng-King Tan
Int. J. Mol. Sci. 2020, 21(23), 9302; https://doi.org/10.3390/ijms21239302 - 06 Dec 2020
Cited by 16 | Viewed by 3076
Abstract
The immune system has been increasingly recognized as a major contributor in the pathogenesis of Parkinson’s disease (PD). The double-edged nature of the immune system poses a problem in harnessing immunomodulatory therapies to prevent and slow the progression of this debilitating disease. To [...] Read more.
The immune system has been increasingly recognized as a major contributor in the pathogenesis of Parkinson’s disease (PD). The double-edged nature of the immune system poses a problem in harnessing immunomodulatory therapies to prevent and slow the progression of this debilitating disease. To tackle this conundrum, understanding the mechanisms underlying immune-mediated neuronal death will aid in the identification of neuroprotective strategies to preserve dopaminergic neurons. Specific innate and adaptive immune mediators may directly or indirectly induce dopaminergic neuronal death. Genetic factors, the gut-brain axis and the recent identification of PD-specific T cells may provide novel mechanistic insights on PD pathogenesis. Future studies to address the gaps in the identification of autoantibodies, variability in immunophenotyping studies and the contribution of gut dysbiosis to PD may eventually provide new therapeutic targets for PD. Full article
(This article belongs to the Special Issue Microglia: On the Cutting Edge between Health and Disease)
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25 pages, 1575 KiB  
Review
Control of Innate Immunity by Sialic Acids in the Nervous Tissue
by Huan Liao, Christine Klaus and Harald Neumann
Int. J. Mol. Sci. 2020, 21(15), 5494; https://doi.org/10.3390/ijms21155494 - 31 Jul 2020
Cited by 18 | Viewed by 6065
Abstract
Sialic acids (Sias) are the most abundant terminal sugar residues of glycoproteins and glycolipids on the surface of mammalian cells. The nervous tissue is the organ with the highest expression level of Sias. The ‘sialylation’ of glycoconjugates is performed via sialyltransferases, whereas ‘desialylation’ [...] Read more.
Sialic acids (Sias) are the most abundant terminal sugar residues of glycoproteins and glycolipids on the surface of mammalian cells. The nervous tissue is the organ with the highest expression level of Sias. The ‘sialylation’ of glycoconjugates is performed via sialyltransferases, whereas ‘desialylation’ is done by sialidases or is a possible consequence of oxidative damage. Sialic acid residues on the neural cell surfaces inhibit complement and microglial activation, as well as phagocytosis of the underlying structures, via binding to (i) complement factor H (CFH) or (ii) sialic acid-binding immunoglobulin-like lectin (SIGLEC) receptors. In contrast, activated microglial cells show sialidase activity that desialylates both microglia and neurons, and further stimulates innate immunity via microglia and complement activation. The desialylation conveys neurons to become susceptible to phagocytosis, as well as triggers a microglial phagocytosis-associated oxidative burst and inflammation. Dysfunctions of the ‘Sia–SIGLEC’ and/or ‘Sia–complement’ axes often lead to neurological diseases. Thus, Sias on glycoconjugates of the intact glycocalyx and its desialylation are major regulators of neuroinflammation. Full article
(This article belongs to the Special Issue Microglia: On the Cutting Edge between Health and Disease)
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13 pages, 310 KiB  
Review
A Fatal Alliance between Microglia, Inflammasomes, and Central Pain
by Stefanie Hoffmann and Cordian Beyer
Int. J. Mol. Sci. 2020, 21(11), 3764; https://doi.org/10.3390/ijms21113764 - 26 May 2020
Cited by 18 | Viewed by 3075
Abstract
Microglia are the resident immune cells in the CNS, which survey the brain parenchyma for pathogens, initiate inflammatory responses, secrete inflammatory mediators, and phagocyte debris. Besides, they play a role in the regulation of brain ion homeostasis and in pruning synaptic contacts and [...] Read more.
Microglia are the resident immune cells in the CNS, which survey the brain parenchyma for pathogens, initiate inflammatory responses, secrete inflammatory mediators, and phagocyte debris. Besides, they play a role in the regulation of brain ion homeostasis and in pruning synaptic contacts and thereby modulating neural networks. More recent work shows that microglia are embedded in brain response related to stress phenomena, the development of major depressive disorders, and pain-associated neural processing. The microglia phenotype varies between activated-toxic-neuroinflammatory to non-activated-protective-tissue remodeling, depending on the challenges and regulatory signals. Increased inflammatory reactions result from brain damage, such as stroke, encephalitis, as well as chronic dysfunctions, including stress and pain. The dimension of damage/toxic stimuli defines the amplitude of inflammation, ranging from an on-off event to low but continuous simmering to uncontrollable. Pain, either acute or chronic, involves inflammasome activation at the point of origin, the different relay stations, and the sensory and processing cortical areas. This short review aimed at identifying a sinister role of the microglia-inflammasome platform for the development and perpetuation of acute and chronic central pain and its association with changes in CNS physiology. Full article
(This article belongs to the Special Issue Microglia: On the Cutting Edge between Health and Disease)
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