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Cells
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Therapeutic Mechanism of Nervous System Inflammation
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Therapeutic Mechanism of Nervous System Inflammation

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

Deadline for manuscript submissions: 15 September 2024 | Viewed by 10375

Special Issue Editors

Prof. Dr. Maria Anttonietta Panaro

E-Mail Website
Guest Editor
Department of Bioscience, Biotechnologies and Environment, University of Bari “Aldo Moro”, Bari, Italy
Interests: neuroinflammation; oxidative stress; neurodegenerative disease; signalling pathways; nutraceutics
Special Issues, Collections and Topics in MDPI journals
Dr. Antonia Cianciulli

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

Special Issue Information

Dear Colleagues,

Neuroinflammation is a process involved in various inflammatory cascades in nervous tissues that can result in persistent and chronic apoptotic neuronal cell death, triggering various degenerative disorders of the central nervous system, including neuroinflammatory and neurodegenerative diseases.

Although neuroinflammation is a natural defense mechanism against a variety of pathologic insults within the central nervous system (CNS), excessive inflammatory responses can be harmful. To contain and repair the local tissue damage, an immediate anti-inflammatory response is required. CNS-resident cells, such as microglia and astrocytes, along with peripheral immune cells, orchestrate a series of events aimed at functional restoration. If the acute inflammatory event is not resolved, it turns toxic, resulting in progressive CNS degeneration. As a result, the cellular, molecular, and biochemical processes that control inflammation must coexist with the intrinsic CNS repair mechanisms that influence tissue healing.

A better understanding of the inflammatory processes that occur prior to or during CNS damage, as well as the subsequent cascades of inflammatory reactions, could lead to the development of novel treatments.

The goal of this Special Issue is to highlight aspects that could potentially contribute as therapeutic interventions to help resolve CNS inflammation, promote tissue repair, and functional recovery after acute injury and infection. Cellular and molecular mechanisms, as well as potential therapeutic targets for inflammatory disorders of the nervous system, will be investigated.

Dr. Maria Antonietta Panaro
Dr. Antonia Cianciulli
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. 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
  • neurodegeneration
  • therapy
  • drug target
  • cell signalling
  • cells of nervous system

Published Papers (4 papers)

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Research

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20 pages, 3668 KiB  
Article
Spatiotemporal Cofilin Signaling, Microglial Activation, Neuroinflammation, and Cognitive Impairment Following Hemorrhagic Brain Injury
by Daniyah A. Almarghalani, Xiaojin Sha, Robert E. Mrak and Zahoor A. Shah
Cells 2023, 12(8), 1153; https://doi.org/10.3390/cells12081153 - 13 Apr 2023
Cited by 5 | Viewed by 1823
Abstract
Intracerebral hemorrhage (ICH) is a significant health concern associated with high mortality. Cofilin plays a crucial role in stress conditions, but its signaling following ICH in a longitudinal study is yet to be ascertained. In the present study, we examined the cofilin expression [...] Read more.
Intracerebral hemorrhage (ICH) is a significant health concern associated with high mortality. Cofilin plays a crucial role in stress conditions, but its signaling following ICH in a longitudinal study is yet to be ascertained. In the present study, we examined the cofilin expression in human ICH autopsy brains. Then, the spatiotemporal cofilin signaling, microglia activation, and neurobehavioral outcomes were investigated in a mouse model of ICH. Human autopsy brain sections from ICH patients showed increased intracellular cofilin localization within microglia in the perihematomal area, possibly associated with microglial activation and morphological changes. Various cohorts of mice were subjected to intrastriatal collagenase injection and sacrificed at time points of 1, 3, 7, 14, 21, and 28 days. Mice suffered from severe neurobehavioral deficits after ICH, lasting for 7 days, followed by a gradual improvement. Mice suffered post-stroke cognitive impairment (PSCI) both acutely and in the chronic phase. Hematoma volume increased from day 1 to 3, whereas ventricle size increased from day 21 to 28. Cofilin protein expression increased in the ipsilateral striatum on days 1 and 3 and then decreased from days 7 to 28. An increase in activated microglia was observed around the hematoma on days 1 to 7, followed by a gradual reduction up to day 28. Around the hematoma, activated microglia showed morphological changes from ramified to amoeboid. mRNA levels of inflammatory [tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and interleukin-6 (IL-6) and anti-inflammatory markers [interleukin-10 (IL-10), transforming growth factor-β TGF-β, and arginase I (Arg1)] increased during the acute phase and decreased in the chronic phase. Blood cofilin levels increased on day 3 and matched the increase in chemokine levels. slingshot protein phosphatase 1 (SSH1) protein, which activates cofilin, was increased from day 1 to 7. These results suggest that microglial activation might be the sequel of cofilin overactivation following ICH, leading to widespread neuroinflammation and consequent PSCI. Full article
(This article belongs to the Special Issue Therapeutic Mechanism of Nervous System Inflammation)
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12 pages, 12727 KiB  
Article
An Efficient Humanized Mouse Model for Oral Anti-Retroviral Administration
by Amber K. Virdi, Sang Ho, Melanie S. Seaton, Arnold Z. Olali, Srinivas D. Narasipura, Hannah J. Barbian, Leannie J. Olivares, Hemil Gonzalez, Lee C. Winchester, Anthony T. Podany, Ryan D. Ross, Lena Al-Harthi and Jennillee Wallace
Cells 2023, 12(7), 1034; https://doi.org/10.3390/cells12071034 - 28 Mar 2023
Cited by 2 | Viewed by 1985
Abstract
HIV anti-retrovirals (ARVs) have vastly improved the life expectancy of people living with HIV (PLWH). However, toxic effects attributed to long-term ARV use also contribute to HIV-related co-morbidities such as heart disease, bone loss and HIV-associated neurocognitive disorders (HAND). Unfortunately, mouse models used [...] Read more.
HIV anti-retrovirals (ARVs) have vastly improved the life expectancy of people living with HIV (PLWH). However, toxic effects attributed to long-term ARV use also contribute to HIV-related co-morbidities such as heart disease, bone loss and HIV-associated neurocognitive disorders (HAND). Unfortunately, mouse models used to study the effects of ARVs on viral suppression, toxicity and HIV latency/tissue reservoirs have not been widely established. Here, we demonstrate an effective mouse model utilizing immune-compromised mice, reconstituted with infected human peripheral blood mononuclear cell (PBMCs). ARVs areincorporated into mouse chow and administered daily with combination ARV regimens includingAtripla (efavirenz, tenofovir disoproxil fumarate, and emtricitabine) and Triumeq (abacavir, dolutegravir and lamivudine). This model measures HIV-infected human cell trafficking, and ARV penetration throughout most relevant HIV organs and plasma, with a large amount of trafficking to the secondary lymphoid organs. Furthermore, the HIV viral load within each organ and the plasma was reduced in ARV treated vs. untreated control. Overall, we have demonstrated a mouse model that is relatively easy and affordable to establish and utilize to study ARVs’ effect on various tissues, including the co-morbid conditions associated with PLWH, such as HAND, and other toxic effects. Full article
(This article belongs to the Special Issue Therapeutic Mechanism of Nervous System Inflammation)
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14 pages, 3018 KiB  
Article
Decoy Receptors Regulation by Resveratrol in Lipopolysaccharide-Activated Microglia
by Rosa Calvello, Chiara Porro, Dario Domenico Lofrumento, Melania Ruggiero, Maria Antonietta Panaro and Antonia Cianciulli
Cells 2023, 12(5), 681; https://doi.org/10.3390/cells12050681 - 21 Feb 2023
Cited by 3 | Viewed by 1266
Abstract
Resveratrol is a polyphenol that acts as antioxidants do, protecting the body against diseases, such as diabetes, cancer, heart disease, and neurodegenerative disorders, such as Alzheimer’s (AD) and Parkinson’s diseases (PD). In the present study, we report that the treatment of activated microglia [...] Read more.
Resveratrol is a polyphenol that acts as antioxidants do, protecting the body against diseases, such as diabetes, cancer, heart disease, and neurodegenerative disorders, such as Alzheimer’s (AD) and Parkinson’s diseases (PD). In the present study, we report that the treatment of activated microglia with resveratrol after prolonged exposure to lipopolysaccharide is not only able to modulate pro-inflammatory responses, but it also up-regulates the expression of decoy receptors, IL-1R2 and ACKR2 (atypical chemokine receptors), also known as negative regulatory receptors, which are able to reduce the functional responses promoting the resolution of inflammation. This result might constitute a hitherto unknown anti-inflammatory mechanism exerted by resveratrol on activated microglia. Full article
(This article belongs to the Special Issue Therapeutic Mechanism of Nervous System Inflammation)
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19 pages, 1452 KiB  
Review
Hypometabolism, Alzheimer’s Disease, and Possible Therapeutic Targets: An Overview
by Snehal Raut, Aditya Bhalerao, Michael Powers, Minelly Gonzalez, Salvatore Mancuso and Luca Cucullo
Cells 2023, 12(16), 2019; https://doi.org/10.3390/cells12162019 - 08 Aug 2023
Cited by 5 | Viewed by 4634
Abstract
The brain is a highly dynamic organ that requires a constant energy source to function normally. This energy is mostly supplied by glucose, a simple sugar that serves as the brain’s principal fuel source. Glucose transport across the blood–brain barrier (BBB) is primarily [...] Read more.
The brain is a highly dynamic organ that requires a constant energy source to function normally. This energy is mostly supplied by glucose, a simple sugar that serves as the brain’s principal fuel source. Glucose transport across the blood–brain barrier (BBB) is primarily controlled via sodium-independent facilitated glucose transport, such as by glucose transporter 1 (GLUT1) and 3 (GLUT3). However, other glucose transporters, including GLUT4 and the sodium-dependent transporters SGLT1 and SGLT6, have been reported in vitro and in vivo. When the BBB endothelial layer is crossed, neurons and astrocytes can absorb the glucose using their GLUT1 and GLUT3 transporters. Glucose then enters the glycolytic pathway and is metabolized into adenosine triphosphate (ATP), which supplies the energy to support cellular functions. The transport and metabolism of glucose in the brain are impacted by several medical conditions, which can cause neurological and neuropsychiatric symptoms. Alzheimer’s disease (AD), Parkinson’s disease (PD), epilepsy, traumatic brain injury (TBI), schizophrenia, etc., are a few of the most prevalent disorders, characterized by a decline in brain metabolism or hypometabolism early in the course of the disease. Indeed, AD is considered a metabolic disorder related to decreased brain glucose metabolism, involving brain insulin resistance and age-dependent mitochondrial dysfunction. Although the conventional view is that reduced cerebral metabolism is an effect of neuronal loss and consequent brain atrophy, a growing body of evidence points to the opposite, where hypometabolism is prodromal or at least precedes the onset of brain atrophy and the manifestation of clinical symptoms. The underlying processes responsible for these glucose transport and metabolic abnormalities are complicated and remain poorly understood. This review article provides a comprehensive overview of the current understanding of hypometabolism in AD and potential therapeutic targets. Full article
(This article belongs to the Special Issue Therapeutic Mechanism of Nervous System Inflammation)
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