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Cells
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Neuron-Glial Interactions in Neurological Diseases
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Neuron-Glial Interactions in Neurological Diseases

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 December 2021) | Viewed by 11072

Special Issue Editor

Dr. Shih-Heng (David) Chen

E-Mail Website
Guest Editor
National Institute of Environmental Health Sciences (NIEHS/NIH), Research Triangle Park, Durham, NC 27709, USA
Interests: neuroimmunology; neuron glia biology; neurodegeneration; gene delivery; gene therapy; viral vectors; virus-cell interactions

Special Issue Information

Dear Colleagues,

In the central nervous system (CNS), the immune response to brain insults is initiated by microglia and astroglia. Due to their different ontogenic origins, microglia and astroglia play different roles during neuroinflammation. Microglia are considered ‘professional’ immune cells due to their myeloid lineage, whereby they can detect and clear pathogens and damaged cells through pattern recognition receptors and phagocytosis. On the other hand, astroglia are derived from a neuroectoderm lineage and assist with maintaining CNS homeostasis, including immune regulation. Neuroinflammatory responses are typically transient and help to restore CNS homeostasis. However, in pathological conditions, neuroinflammation may continue unresolved, becoming persistent. Damaged neurons release endogenous proteins and cell membrane fragments that can re-stimulate the activation of microglia forming a chronic state of activation known as reactive microgliosis. Although reactive gliosis is the hallmark of neuropathological conditions, the mechanisms of how neuron–glial interact during neuroinflammation are not fully understood.

In this Special Issue, we aim to publish commentaries, original research articles, and reviews in the area of (1) neuron–glial interactions in healthy or diseased conditions; (2) molecular mechanisms of chronic neuroinflammation; and (3) the potential interventions to neuroinflammation. I am convinced that this Special Issue of Cells will unveil the mechanisms of neuron–glial interactions in neurological diseases and inspire the development of potential therapies. I look forward to your contributions to this Special Issue.

Dr. Shih-Heng (David) Chen
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

  • microglia
  • astroglia
  • neuroinflammation
  • neurodegeneration
  • neuron–glial interaction

Published Papers (4 papers)

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Research

19 pages, 3519 KiB  
Article
Inhibition of Nigral Microglial Activation Reduces Age-Related Loss of Dopaminergic Neurons and Motor Deficits
by Tzu-Feng Wang, Shih-Ying Wu, Bo-Syong Pan, Sheng-Feng Tsai and Yu-Min Kuo
Cells 2022, 11(3), 481; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11030481 - 30 Jan 2022
Cited by 6 | Viewed by 2835
Abstract
Parkinson’s disease (PD) is an age-related neurodegenerative disease caused by a selective loss of dopaminergic (DA) neurons in the substantia nigra (SN). Microglial activation is implicated in the pathogenesis of PD. This study aimed to characterize the role of microglial activation in aging-related [...] Read more.
Parkinson’s disease (PD) is an age-related neurodegenerative disease caused by a selective loss of dopaminergic (DA) neurons in the substantia nigra (SN). Microglial activation is implicated in the pathogenesis of PD. This study aimed to characterize the role of microglial activation in aging-related nigral DA neuron loss and motor deficits in mice. We showed that, compared to 3-month-old mice, the number of DA neurons in the SN and the expression of dopamine transporter (DAT) in the striatum decreased during the period of 9 to 12 months of age. Motor deficits and microglial activation in the SN were also evident during these months. The number of DA neurons was negatively correlated with the degrees of microglial activation. The inhibition of age-related microglial activation by ibuprofen during these 3 months decreased DA neuron loss in the SN. Eliminating the microglia prevented systemic inflammation-induced DA neuron death. Forcing mice to run during these 3 months inhibited microglial activation and DA neuron loss. Blocking the brain-derived neurotrophic factor (BDNF) signaling eliminated the exercise-induced protective effects. In conclusion, nigral DA neurons were susceptible to local microglial activation. Running exercise upregulated BDNF-TrkB signaling and inhibited microglial activation during aging. Long-term exercise can be considered as a non-pharmacological strategy to ameliorate microglial activation and related neurodegeneration. Full article
(This article belongs to the Special Issue Neuron-Glial Interactions in Neurological Diseases)
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18 pages, 3385 KiB  
Article
2-PMAP Ameliorates Cerebral Vasospasm and Brain Injury after Subarachnoid Hemorrhage by Regulating Neuro-Inflammation in Rats
by Chieh-Hsin Wu, Hung-Pei Tsai, Yu-Feng Su, Cheng-Yu Tsai, Ying-Yi Lu and Chih-Lung Lin
Cells 2022, 11(2), 242; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11020242 - 12 Jan 2022
Cited by 4 | Viewed by 2002
Abstract
A subarachnoid hemorrhage (SAH), leading to severe disability and high fatality in survivors, is a devastating disease. Neuro-inflammation, a critical mechanism of cerebral vasospasm and brain injury from SAH, is tightly related to prognoses. Interestingly, studies indicate that 2-[(pyridine-2-ylmethyl)-amino]-phenol (2-PMAP) crosses the blood–brain [...] Read more.
A subarachnoid hemorrhage (SAH), leading to severe disability and high fatality in survivors, is a devastating disease. Neuro-inflammation, a critical mechanism of cerebral vasospasm and brain injury from SAH, is tightly related to prognoses. Interestingly, studies indicate that 2-[(pyridine-2-ylmethyl)-amino]-phenol (2-PMAP) crosses the blood–brain barrier easily. Here, we investigated whether the vasodilatory and neuroprotective roles of 2-PMAP were observed in SAH rats. Rats were assigned to three groups: sham, SAH and SAH+2-PMAP. SAHs were induced by a cisterna magna injection. In the SAH+2-PMAP group, 5 mg/kg 2-PMAP was injected into the subarachnoid space before SAH induction. The administration of 2-PMAP markedly ameliorated cerebral vasospasm and decreased endothelial apoptosis 48 h after SAH. Meanwhile, 2-PMAP decreased the severity of neurological impairments and neuronal apoptosis after SAH. Furthermore, 2-PMAP decreased the activation of microglia and astrocytes, expressions of TLR-4 and p-NF-κB, inflammatory markers (TNF-α, IL-1β and IL-6) and reactive oxygen species. This study is the first to confirm that 2-PMAP has vasodilatory and neuroprotective effects in a rat model of SAH. Taken together, the experimental results indicate that 2-PMAP treatment attenuates neuro-inflammation, oxidative stress and cerebral vasospasm, in addition to ameliorating neurological deficits, and that these attenuating and ameliorating effects are conferred through the TLR-4/NF-κB pathway. Full article
(This article belongs to the Special Issue Neuron-Glial Interactions in Neurological Diseases)
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17 pages, 3766 KiB  
Article
Polarization of Type 1 Macrophages Is Associated with the Severity of Viral Encephalitis Caused by Japanese Encephalitis Virus and Dengue Virus
by Ming-Kai Jhan, Chia-Ling Chen, Ting-Jing Shen, Po-Chun Tseng, Yung-Ting Wang, Rahmat Dani Satria, Chia-Yi Yu and Chiou-Feng Lin
Cells 2021, 10(11), 3181; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10113181 - 15 Nov 2021
Cited by 12 | Viewed by 2869
Abstract
Infection with flaviviruses causes mild to severe diseases, including viral hemorrhagic fever, vascular shock syndrome, and viral encephalitis. Several animal models explore the pathogenesis of viral encephalitis, as shown by neuron destruction due to neurotoxicity after viral infection. While neuronal cells are injuries [...] Read more.
Infection with flaviviruses causes mild to severe diseases, including viral hemorrhagic fever, vascular shock syndrome, and viral encephalitis. Several animal models explore the pathogenesis of viral encephalitis, as shown by neuron destruction due to neurotoxicity after viral infection. While neuronal cells are injuries caused by inflammatory cytokine production following microglial/macrophage activation, the blockade of inflammatory cytokines can reduce neurotoxicity to improve the survival rate. This study investigated the involvement of macrophage phenotypes in facilitating CNS inflammation and neurotoxicity during flavivirus infection, including the Japanese encephalitis virus, dengue virus (DENV), and Zika virus. Mice infected with different flaviviruses presented encephalitis-like symptoms, including limbic seizure and paralysis. Histology indicated that brain lesions were identified in the hippocampus and surrounded by mononuclear cells. In those regions, both the infiltrated macrophages and resident microglia were significantly increased. RNA-seq analysis showed the gene profile shifting toward type 1 macrophage (M1) polarization, while M1 markers validated this phenomenon. Pharmacologically blocking C-C chemokine receptor 2 and tumor necrosis factor-α partly retarded DENV-induced M1 polarization. In summary, flavivirus infection, such as JEV and DENV, promoted type 1 macrophage polarization in the brain associated with encephalitic severity. Full article
(This article belongs to the Special Issue Neuron-Glial Interactions in Neurological Diseases)
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13 pages, 2856 KiB  
Article
Early-Released Interleukin-10 Significantly Inhibits Lipopolysaccharide-Elicited Neuroinflammation In Vitro
by Yubao Wang, Pei Yu, Yi Li, Zhan Zhao, Xiaomei Wu, Lu Zhang, Jing Feng and Jau-Shyong Hong
Cells 2021, 10(9), 2173; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10092173 - 24 Aug 2021
Cited by 6 | Viewed by 2611
Abstract
Anti-inflammatory cytokine interleukin (IL)-10 is pivotal for limiting excessive inflammation in the central nervous system. Reports show that lipopolysaccharide (LPS)-induced microglial IL-10 emerges in a delayed manner in vitro and in vivo, lagging behind proinflammatory cytokines to facilitate the resolution of neuroinflammation. We [...] Read more.
Anti-inflammatory cytokine interleukin (IL)-10 is pivotal for limiting excessive inflammation in the central nervous system. Reports show that lipopolysaccharide (LPS)-induced microglial IL-10 emerges in a delayed manner in vitro and in vivo, lagging behind proinflammatory cytokines to facilitate the resolution of neuroinflammation. We hypothesized that IL-10 releases quite quickly based on our pilot investigation. Here, we uncovered a bimodal expression of microglial IL-10 gene transcription induced by LPS in mouse primary mixed glial cultures. This pattern consisted of a short brief early-phase and a long-lived late-phase, enabling the production of IL-10 protein in a rapid manner. The removal and addition of IL-10 protein assays indicated that early-released IL-10 exerted potent modulatory effects on neuroinflammation at picomolar levels, and IL-10 released at the onset of neuroinflammation is tightly controlled. We further showed that the early-released, but not the late-released, IL-10 was crucial for mediating and potentiating the anti-inflammatory function of a β2-adrenergic receptor agonist salmeterol. This study in vitro highlights the essential role of early-released IL-10 in regulating the appropriate degree of neuroinflammation, overturning the previous notion that microglial IL-10 produces and functions in a delayed manner and providing new insights into anti-inflammatory mechanisms-mediated neuroimmune homeostasis. Full article
(This article belongs to the Special Issue Neuron-Glial Interactions in Neurological Diseases)
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