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Cells
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Glia Cells in Inflammation
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Glia Cells in Inflammation

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

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 12599

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,

The main effector cells of the innate immune response within the CNS are glial cells, in particular microglia and astrocytes. Resident microglia and astrocytes exert multiple functions including protective and restorative effects in response to CNS infection, injury, or neurodegenerative diseases. Numerous findings indicate that inflammation can promote the progression of these disorders. Glial cells play a significant role in the development of inflammation in the CNS, but many aspects of this process are not yet understood. In recent years, the question of the interaction of glial cells with the periphery and vice versa has become increasingly important. The interaction seems to be particularly important in the development of glial cells and the establishment of a functioning immune defense in the CNS. This Special Issue seeks reviews and original papers covering a wide range of topics related to studies around the role of glial cells in inflammation in the CNS and also its periphery (e.g., brain–gut axis), which show the development of new models or therapeutic approaches or the role of interesting factors in influencing glial cells in various disorders. Research from in vitro and in vivo studies will be considered.

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

  • astrocyte
  • microglial cell
  • glia cell
  • inflammation
  • neurodegeneration
  • immune response
  • neuroprotection
  • CNS

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Published Papers (3 papers)

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Research

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19 pages, 3068 KiB  
Article
Aquaporin-4 Expression during Toxic and Autoimmune Demyelination
by Sven Olaf Rohr, Theresa Greiner, Sarah Joost, Sandra Amor, Paul van der Valk, Christoph Schmitz and Markus Kipp
Cells 2020, 9(10), 2187; https://doi.org/10.3390/cells9102187 - 28 Sep 2020
Cited by 19 | Viewed by 3428
Abstract
The water channel protein aquaporin-4 (AQP4) is required for a normal rate of water exchange across the blood–brain interface. Following the discovery that AQP4 is a possible autoantigen in neuromyelitis optica, the function of AQP4 in health and disease has become a research [...] Read more.
The water channel protein aquaporin-4 (AQP4) is required for a normal rate of water exchange across the blood–brain interface. Following the discovery that AQP4 is a possible autoantigen in neuromyelitis optica, the function of AQP4 in health and disease has become a research focus. While several studies have addressed the expression and function of AQP4 during inflammatory demyelination, relatively little is known about its expression during non-autoimmune-mediated myelin damage. In this study, we used the toxin-induced demyelination model cuprizone as well as a combination of metabolic and autoimmune myelin injury (i.e., Cup/EAE) to investigate AQP4 pathology. We show that during toxin-induced demyelination, diffuse AQP4 expression increases, while polarized AQP4 expression at the astrocyte endfeet decreases. The diffuse increased expression of AQP4 was verified in chronic-active multiple sclerosis lesions. Around inflammatory brain lesions, AQP4 expression dramatically decreased, especially at sites where peripheral immune cells penetrate the brain parenchyma. Humoral immune responses appear not to be involved in this process since no anti-AQP4 antibodies were detected in the serum of the experimental mice. We provide strong evidence that the diffuse increase in anti-AQP4 staining intensity is due to a metabolic injury to the brain, whereas the focal, perivascular loss of anti-AQP4 immunoreactivity is mediated by peripheral immune cells. Full article
(This article belongs to the Special Issue Glia Cells in Inflammation)
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32 pages, 4606 KiB  
Article
Maternal Immune Activation Sensitizes Male Offspring Rats to Lipopolysaccharide-Induced Microglial Deficits Involving the Dysfunction of CD200–CD200R and CX3CL1–CX3CR1 Systems
by Katarzyna Chamera, Magdalena Szuster-Głuszczak, Ewa Trojan and Agnieszka Basta-Kaim
Cells 2020, 9(7), 1676; https://doi.org/10.3390/cells9071676 - 12 Jul 2020
Cited by 24 | Viewed by 4092
Abstract
Early life challenges resulting from maternal immune activation (MIA) may exert persistent effects on the offspring, including the development of psychiatric disorders, such as schizophrenia. Recent evidence has suggested that the adverse effects of MIA may be mediated by neuron–microglia crosstalk, particularly CX3CL1–CX3CR1 [...] Read more.
Early life challenges resulting from maternal immune activation (MIA) may exert persistent effects on the offspring, including the development of psychiatric disorders, such as schizophrenia. Recent evidence has suggested that the adverse effects of MIA may be mediated by neuron–microglia crosstalk, particularly CX3CL1–CX3CR1 and CD200–CD200R dyads. Therefore, the present study assessed the behavioural parameters resembling schizophrenia-like symptoms in the adult male offspring of Sprague-Dawley rats that were exposed to MIA and to an additional acute lipopolysaccharide (LPS) challenge in adulthood, according to the “two-hit” hypothesis of schizophrenia. Simultaneously, we aimed to clarify the role of the CX3CL1–CX3CR1 and CD200–CD200R axes and microglial reactivity in the brains of adult offspring subjected to MIA and the “second hit” wit LPS. In the present study, MIA generated a range of behavioural changes in the adult male offspring, including increased exploratory activity and anxiety-like behaviours. The most intriguing finding was observed in the prepulse inhibition (PPI) test, where the deficit in the sensorimotor gating was age-dependent and present only in part of the rats. We were able to distinguish the occurrence of two groups: responsive and non-responsive (without the deficit). Concurrently, based on the results of the biochemical studies, MIA disrupted mainly the CD200–CD200R system, while the changes of the CX3CL1–CX3CR1 axis were less evident in the frontal cortex of adult non-responsive offspring. MIA markedly affected the immune regulators of the CD200–CD200R pathway as we observed an increase in cortical IL-6 release in the responsive group and IL-4 in the non-responsive offspring. Importantly, the “second hit” generated disturbances at the behavioural and biochemical levels mostly in the non-responsive adult animals. Those offspring were characterized both by disturbed PPI and “priming” microglia. Altogether, the exposure to MIA altered the immunomodulatory mechanisms, including the CD200–CD200R axis, in the brain and sensitized animals to subsequent immunological challenges, leading to the manifestation of schizophrenia-like alterations. Full article
(This article belongs to the Special Issue Glia Cells in Inflammation)
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Review

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17 pages, 1652 KiB  
Review
Does Siponimod Exert Direct Effects in the Central Nervous System?
by Markus Kipp
Cells 2020, 9(8), 1771; https://doi.org/10.3390/cells9081771 - 24 Jul 2020
Cited by 23 | Viewed by 4249
Abstract
The modulation of the sphingosine 1-phosphate receptor is an approved treatment for relapsing multiple sclerosis because of its anti-inflammatory effect of retaining lymphocytes in lymph nodes. Different sphingosine 1-phosphate receptor subtypes are expressed in the brain and spinal cord, and their pharmacological effects [...] Read more.
The modulation of the sphingosine 1-phosphate receptor is an approved treatment for relapsing multiple sclerosis because of its anti-inflammatory effect of retaining lymphocytes in lymph nodes. Different sphingosine 1-phosphate receptor subtypes are expressed in the brain and spinal cord, and their pharmacological effects may improve disease development and neuropathology. Siponimod (BAF312) is a novel sphingosine 1-phosphate receptor modulator that has recently been approved for the treatment of active secondary progressive multiple sclerosis (MS). In this review article, we summarize recent evidence suggesting that the active role of siponimod in patients with progressive MS may be due to direct interaction with central nervous system cells. Additionally, we tried to summarize our current understanding of the function of siponimod and discuss the effects observed in the case of MS. Full article
(This article belongs to the Special Issue Glia Cells in Inflammation)
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