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Neuroglia
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New Insights into the Anti-inflammatory Role of Microglia
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New Insights into the Anti-inflammatory Role of Microglia

A special issue of Neuroglia (ISSN 2571-6980).

Deadline for manuscript submissions: closed (15 December 2023) | Viewed by 7206

Special Issue Editor

Dr. Antonia Cianciulli

E-Mail Website
Guest Editor
Department of Bioscience, Biotechnologies and Biopharmaceutics, University of Bari “Aldo Moro”, Bari, Italy
Interests: neuroinflammation; signaling; bioactive compounds; evolutionary computational study
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Microglia are the immune-competent cells of the CNS and are highly similar to peripheral macrophages. They act as the major inflammatory cell type in the brain responding to pathogens and injury. Microglia, for this reason, are considered as key players in the pathogenesis of multiple neurodegenerative and chronic neuroinflammatory diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS).

There are accumulating data that suggest the existence of two competing populations of microglia. A neurotoxic and overactivated microglia population involved in promoting the loss of synapses and neurons and a pro-regenerative and neuroprotective microglia population capable of reducing disease progression and to promote the establishment of a brain healing environment. Microglial cells belonging to these two populations can release cytokines and other mediators that support and direct the immune response. In particular, the pro-regenerative microglia population seems that could also be instrumental in resolving the inflammatory response through the production of anti-inflammatory mediators and anti-inflammatory cytokines, such as IL-10. Recent studies strongly highlight that manipulation of microglial activation can affect the progression of neurodegenerative and chronic neuroinflammatory diseases modifying systemic inflammatory processes.

Outlining the mechanisms involved in balancing microglial responses could be a promising way to develop novel therapeutic strategies for inflammatory brain diseases. The purpose of this Special Issue is to receive original research articles and reviews that focus on unraveling the role of the anti-inflammatory population of microglia by providing new insight into the current understanding of inflammatory based brain diseases. Manuscripts addressing the deepening of the role of anti-inflammatory microglia in brain aging, as well as in aged brains are also well accepted.

Dr. Antonia Cianciulli
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. Neuroglia is an international peer-reviewed open access quarterly 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 1000 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
  • neurodegeneration
  • neuroimmunomodulation
  • glia cell
  • microglial cell
  • brain protection

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Published Papers (2 papers)

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16 pages, 4441 KiB  
Article
A Human Microglial Cell Line Expresses γ-Aminobutyric Acid (GABA) Receptors and Responds to GABA and Muscimol by Increasing Production of IL-8
by Ashley Wagner, Zhimin Yan and Marianna Kulka
Neuroglia 2023, 4(3), 172-187; https://doi.org/10.3390/neuroglia4030012 - 28 Jun 2023
Viewed by 2718
Abstract
Gamma-aminobutyric acid (GABA) is an essential neurotransmitter and an important regulator of neuroinflammation and disease. Microglia are important immune cells in the brain that express GABA receptors (GABAR) and respond to both GABA and GABAR agonists, yet the effect of GABA on microglial [...] Read more.
Gamma-aminobutyric acid (GABA) is an essential neurotransmitter and an important regulator of neuroinflammation and disease. Microglia are important immune cells in the brain that express GABA receptors (GABAR) and respond to both GABA and GABAR agonists, yet the effect of GABA on microglial inflammatory responses is unclear. We hypothesized that GABA and GABAR agonists might modify the activation of a human microglial cell line (HMC3). We further hypothesized that Amanita muscaria extract (AME-1), which contained GABAR agonists (GABA and muscimol), would similarly stimulate HMC3. Ligand-gated GABAR (GABAAR) and G protein-coupled GABAR (GABABR) subunit expression was analyzed by qRT-PCR, metabolic activity was determined by nicotinamide adenine dinucleotide (NADH)-dependent oxidoreductase assay (XTT), reactive oxygen species (ROS) generation was analyzed by 2′,7′-dichlorodihydrofluorescein diacetate (DCFDA), and interleukin-8 (IL-8) production was analyzed by an enzyme-linked immunosorbent assay (ELISA). HMC3 expressed several neuroreceptors such as subunits of the GABAA receptor (GABAAR). HMC3 constitutively produce IL-8 and ROS. Both muscimol and GABA stimulated HMC3 to produce more IL-8 but had no effect on constitutive ROS production. GABA and muscimol altered the morphology and Iba1 localization of HMC3. GABA, but not muscimol, increased HMC3 metabolic activity. Similarly, AME-1 induced HMC3 to produce more IL-8 but not ROS and altered cell morphology and Iba1 localization. GABA induction of IL-8 was blocked by bicuculline, an antagonist of GABAAR. AME-1-induced production of IL-8 was not blocked by bicuculline, suggesting that AME-1’s effect on HMC3 was independent of GABAAR. In conclusion, these data show that GABA and GABA agonists stimulate HMC3 to increase their production of IL-8. Mixtures that contain GABA and muscimol, such as AME-1, have similar effects on HMC3 that are independent of GABAAR. Full article
(This article belongs to the Special Issue New Insights into the Anti-inflammatory Role of Microglia)
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22 pages, 1155 KiB  
Perspective
The Role of Lactylation in Mental Illness: Emphasis on Microglia
by Adonis Sfera, Carolina Klein, Johnathan J. Anton, Zisis Kozlakidis and Christina V. Andronescu
Neuroglia 2023, 4(2), 119-140; https://doi.org/10.3390/neuroglia4020009 - 16 May 2023
Cited by 3 | Viewed by 3262
Abstract
A paradigm shift is currently taking place in the etiopathogenesis of neuropsychiatric disorders as immunometabolism is replacing the earlier neurotransmitter model. According to the new concept, cellular bioenergetics drives information processing in the central nervous system; therefore, neuropathology is conceptualized as a direct [...] Read more.
A paradigm shift is currently taking place in the etiopathogenesis of neuropsychiatric disorders as immunometabolism is replacing the earlier neurotransmitter model. According to the new concept, cellular bioenergetics drives information processing in the central nervous system; therefore, neuropathology is conceptualized as a direct consequence of impaired metabolism. Along the same lines, endoplasmic reticulum stress and gut barrier dysfunction are emerging as novel targets in schizophrenia and affective disorders, linking immune responses to cellular distress. Furthermore, microglia, the brain’s innate immune cells, acquire energy through oxidative phosphorylation, while in the resting state, and glycolysis upon activation, contributing to lactate accumulation and reduced brain pH. The same metabolic signature characterizes neuropsychiatric disorders as the central nervous system derives adenosine triphosphate from aerobic glycolysis, upregulating lactate and generating an acidic environment. Although known for over three decades, the link between dysmetabolism and neuropathology was poorly defined until the discovery of brain-resident innate lymphoid cells, including natural killer cells, and lactylation of histone and nonhistone proteins. In this perspective article, we examine three anti-inflammatory microglial systems relevant for neuropsychiatry: lactate, oxytocin, and the aryl hydrocarbon receptor. We also discuss potential interventions for restoring microglial homeostasis. Full article
(This article belongs to the Special Issue New Insights into the Anti-inflammatory Role of Microglia)
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