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Cells
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Behind and beyond Neuroinflammation: State of the Art and New Perspectives
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Behind and beyond Neuroinflammation: State of the Art and New Perspectives

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 (30 November 2024) | Viewed by 5838

Special Issue Editors

Dr. Daniele Nosi

E-Mail Website
Guest Editor
Dipartimento di Medicina Sperimentale e Clinica, Università degli Studi di Firenze, Largo Brambilla 3, 50134 Firenze, Italy
Interests: neuroinflammation; astrocyte-microglia interplay; neurodegeneration; amyloid proteins; cell membrane
Special Issues, Collections and Topics in MDPI journals
Dr. Jacopo Junio Valerio Branca

E-Mail Website
Guest Editor
Department of Experimental and Clinical Medicine, Anatomy Section, School of Human Health Sciences, University of Florence, 50121 Florence, Italy
Interests: blood–brain barrier; vitamin D; cadmium toxicity; cannabidiol; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation is currently considered a hallmark of most neurological disorders, consisting of the collective dynamic response of glial cells to impaired nervous tissue homeostasis. The reactivities of astrocytes and

microglia are characterized by a wide spectrum of phenotypes that, in chronic diseases, may shift from neuroprotective to neurotoxic. It is known that the reactivity of glial cells is modulated by environmental conditions, including both the chemical and physical properties of the extracellular matrix, and

intense signaling reverberating among different cell types. According to an emerging idea, all cells in the nervous system are, indeed, connected by an intricate network of mutual influences and interdependencies, where intercellular interactions represent links and nodes. A deeper knowledge of the properties of this network, including the mechanisms that promote collective responses to different challenges, in both normal and pathological conditions, could help to understand some of the most controversial features of neuroinflammation.

This Special Issue fits this two-fold perspective; it is dedicated to research that can increase the current knowledge of cell interactions in neuroinflammation and their role in normal conditions. In addition, studies regarding how these interactions are affected by, or may affect, the extracellular matrix will also be considered for publication. This could inspire the concept of the nervous tissue as a microsystem, whose properties are affected by lifespan adaptations to a changing microenvironment.

Dr. Daniele Nosi
Dr. Jacopo Junio Valerio Branca
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

  • astrocytes
  • microglia
  • neurons
  • intercellular interactions
  • neurodegeneration
  • neuroprotection
  • extracellular matrix

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Related Special Issue

Published Papers (3 papers)

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Research

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30 pages, 40572 KiB  
Article
Sex Dependent Disparities in the Central Innate Immune Response after Moderate Spinal Cord Contusion in Rat
by Mousumi Ghosh, Jinyoung Lee, Ashley N. Burke, Thomas A. Strong, Jacqueline Sagen and Damien D. Pearse
Cells 2024, 13(7), 645; https://doi.org/10.3390/cells13070645 - 6 Apr 2024
Cited by 3 | Viewed by 2237
Abstract
Subacute spinal cord injury (SCI) displays a complex pathophysiology associated with pro-inflammation and ensuing tissue damage. Microglia, the resident innate immune cells of the CNS, in concert with infiltrating macrophages, are the primary contributors to SCI-induced inflammation. However, subpopulations of activated microglia can [...] Read more.
Subacute spinal cord injury (SCI) displays a complex pathophysiology associated with pro-inflammation and ensuing tissue damage. Microglia, the resident innate immune cells of the CNS, in concert with infiltrating macrophages, are the primary contributors to SCI-induced inflammation. However, subpopulations of activated microglia can also possess immunomodulatory activities that are essential for tissue remodeling and repair, including the production of anti-inflammatory cytokines and growth factors that are vital for SCI recovery. Recently, reports have provided convincing evidence that sex-dependent differences exist in how microglia function during CNS pathologies and the extent to which these cells contribute to neurorepair and endogenous recovery. Herein we employed flow cytometry and immunohistochemical methods to characterize the phenotype and population dynamics of activated innate immune cells within the injured spinal cord of age-matched male and female rats within the first week (7 days) following thoracic SCI contusion. This assessment included the analysis of pro- and anti-inflammatory markers, as well as the expression of critical immunomodulatory kinases, including P38 MAPK, and transcription factors, such as NFκB, which play pivotal roles in injury-induced inflammation. We demonstrate that activated microglia from the injured spinal cord of female rats exhibited a significantly diminutive pro-inflammatory response, but enhanced anti-inflammatory activity compared to males. These changes included lower levels of iNOS and TLR4 expression but increased levels of ARG-1 and CD68 in females after SCI. The altered expression of these markers is indicative of a disparate secretome between the microglia of males and females after SCI and that the female microglia possesses higher phagocytic capabilities (increased CD68). The examination of immunoregulatory kinases and transcription factors revealed that female microglia had higher levels of phosphorylated P38Thr180/Tyr182 MAPK and nuclear NFκB pp50Ser337 but lower amounts of nuclear NFκB pp65Ser536, suggestive of an attenuated pro-inflammatory phenotype in females compared to males after SCI. Collectively, this work provides novel insight into some of the sex disparities that exist in the innate immune response after SCI and indicates that sex is an important variable when designing and testing new therapeutic interventions or interpretating positive or negative responses to an intervention. Full article
(This article belongs to the Special Issue Behind and beyond Neuroinflammation: State of the Art and New Perspectives)
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Review

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32 pages, 5152 KiB  
Review
From Homeostasis to Neuroinflammation: Insights into Cellular and Molecular Interactions and Network Dynamics
by Ludmila Müller, Svetlana Di Benedetto and Viktor Müller
Cells 2025, 14(1), 54; https://doi.org/10.3390/cells14010054 - 5 Jan 2025
Cited by 3 | Viewed by 1943
Abstract
Neuroinflammation is a complex and multifaceted process that involves dynamic interactions among various cellular and molecular components. This sophisticated interplay supports both environmental adaptability and system resilience in the central nervous system (CNS) but may be disrupted during neuroinflammation. In this article, we [...] Read more.
Neuroinflammation is a complex and multifaceted process that involves dynamic interactions among various cellular and molecular components. This sophisticated interplay supports both environmental adaptability and system resilience in the central nervous system (CNS) but may be disrupted during neuroinflammation. In this article, we first characterize the key players in neuroimmune interactions, including microglia, astrocytes, neurons, immune cells, and essential signaling molecules such as cytokines, neurotransmitters, extracellular matrix (ECM) components, and neurotrophic factors. Under homeostatic conditions, these elements promote cellular cooperation and stability, whereas in neuroinflammatory states, they drive adaptive responses that may become pathological if dysregulated. We examine how neuroimmune interactions, mediated through these cellular actors and signaling pathways, create complex networks that regulate CNS functionality and respond to injury or inflammation. To further elucidate these dynamics, we provide insights using a multilayer network (MLN) approach, highlighting the interconnected nature of neuroimmune interactions under both inflammatory and homeostatic conditions. This perspective aims to enhance our understanding of neuroimmune communication and the mechanisms underlying shifts from homeostasis to neuroinflammation. Applying an MLN approach offers a more integrative view of CNS resilience and adaptability, helping to clarify inflammatory processes and identify novel intervention points within the layered landscape of neuroinflammatory responses. Full article
(This article belongs to the Special Issue Behind and beyond Neuroinflammation: State of the Art and New Perspectives)
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15 pages, 2976 KiB  
Review
Alzheimer’s Disease: In Vitro and In Vivo Evidence of Activation of the Plasma Bradykinin-Forming Cascade and Implications for Therapy
by Allen P. Kaplan, Berhane Ghebrehiwet and Kusumam Joseph
Cells 2024, 13(24), 2039; https://doi.org/10.3390/cells13242039 - 10 Dec 2024
Viewed by 1023
Abstract
The plaques associated with Alzheimer’s disease are formed as a result of the aggregation of Aβ peptides, which vary in length from 38 to 43 amino acids. The 1-40 peptide is the most abundant, while the 1-42 peptide appears to be the most [...] Read more.
The plaques associated with Alzheimer’s disease are formed as a result of the aggregation of Aβ peptides, which vary in length from 38 to 43 amino acids. The 1-40 peptide is the most abundant, while the 1-42 peptide appears to be the most destructive to neurons and/or glial cells in a variety of assays. We have demonstrated that aggregated Aβ, a state prior to plaque formation, will activate the plasma bradykinin-forming pathway when tested in vitro. Aggregation is zinc-dependent, optimal at 25–50 µM, and the rate of aggregation is paralleled by the rate of activation of the bradykinin-forming pathway as assessed by plasma kallikrein formation. The aggregation of Aβ 1-38, 1-40, and 1-42 is optimal after incubation for 3 days, 3 h, and under 1 min, respectively. The cascade is initiated by the autoactivation of factor XII upon binding to aggregated Aβ; then, prekallikrein is converted to kallikrein, which cleaves high-molecular-weight kininogen (HK) to release bradykinin. Studies by a variety of other researchers have demonstrated the presence of each “activation-step” in either the plasma or spinal fluid of patients with Alzheimer’s disease, including activated factor XII, kallikrein, and bradykinin itself. There is also evidence that activation is more prominent as dementia worsens. We now have medications that can block each step of the bradykinin-forming pathway as currently employed for the therapy of hereditary angioedema. Given the current state of therapy for Alzheimer’s disease, which includes monoclonal antibodies that retard the rate of progression by 30% at most and have significant side effects, it seems imperative to explore prophylaxis using one of the long-acting agents that target plasma kallikrein or factor XIIa. There is a long-acting bradykinin antagonist in development, and techniques to target kallikrein mRNA to lower levels or knock out the prekallikrein gene are being developed. Full article
(This article belongs to the Special Issue Behind and beyond Neuroinflammation: State of the Art and New Perspectives)
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