Therapeutic Mechanism of Nervous System Inflammation—Second Edition

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

Deadline for manuscript submissions: 10 December 2025 | Viewed by 1386

Special Issue Editors


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,

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 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 enable 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.

Prof. Dr. Maria Anttonietta 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 signaling
  • cells of nervous system

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issue

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

14 pages, 1264 KiB  
Article
Chronic Pain Induced by Social Defeat Stress in Juvenile Mice Depends on TLR4
by Julia Borges Paes Lemes, Alisa Panichkina, Kaue Franco Malange, Carlos E. Morado-Urbina, Sara Anna Dochnal, Saee Jadhav, Maksim Dolmat, Marco Pagliusi, Jr., Juliana M. Navia-Pealez, Maripat Corr, Yury I. Miller and Tony L. Yaksh
Cells 2025, 14(5), 350; https://doi.org/10.3390/cells14050350 - 27 Feb 2025
Viewed by 1054
Abstract
A significant portion of adolescents suffer from mental illnesses and persistent pain due to repeated stress. The components of the nervous system that link stress and pain in early life remain unclear. Prior studies in adult mice implicated the innate immune system, specifically [...] Read more.
A significant portion of adolescents suffer from mental illnesses and persistent pain due to repeated stress. The components of the nervous system that link stress and pain in early life remain unclear. Prior studies in adult mice implicated the innate immune system, specifically Toll-like receptors (TLRs), as critical for inducing long-term anxiety and pain-like behaviors in social defeat stress (SDS) models. In this work, we investigated the pain and anxiety behavioral phenotypes of wild-type and TLR4-deficient juvenile mice subjected to repeated SDS and evaluated the engagement of TLR4 by measuring dimerization in the spinal cord, dorsal root ganglia, and prefrontal cortex. Male juvenile (4-week-old) mice (C57BL/6J or Tlr4-/-) underwent six social defeat sessions with adult aggressor (CD1) mice. In WT mice, SDS promotes chronic mechanical allodynia and thermal hyperalgesia assessed via von Frey testing and the Hargreaves test, respectively. In parallel, the stressed WT mice exhibited transient anxiety-like behavior and long-lasting locomotor activity reduction in the open-field test. Tlr4-/--stressed animals were resistant to the induction of pain-like behavior but had a remnant of anxious behavior, spending less time in the center of the arena. In WT SDS, there were concordant robust increases in TLR4 dimerization in dorsal root ganglia macrophages and spinal cord microglia, indicating TLR4 activation. These results suggest that the chronic pain phenotype and locomotor impairment induced by SDS in juvenile mice depends on TLR4 engagement evidenced by dimerization in immune cells of the dorsal root ganglia and spinal cord. Full article
(This article belongs to the Special Issue Therapeutic Mechanism of Nervous System Inflammation—Second Edition)
Show Figures

Graphical abstract

Back to TopTop