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Brain Sciences
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Advances in Neuroinflammation and Immune Response
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Advances in Neuroinflammation and Immune Response

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Systems Neuroscience".

Deadline for manuscript submissions: closed (28 February 2026) | Viewed by 1320

Special Issue Editor

Dr. Bojan Shutinoski

E-Mail Website
Guest Editor
Bureau of Microbial Hazards, Health Canada, Ottawa, ON K1A 0K9, Canada
Interests: neurodegeneration; immunology; neuroinflammation

Special Issue Information

Dear Colleagues,

This Special Issue, “Advances in Neuroinflammation and Immune Response” in Brain Sciences, highlights cutting-edge research focused on the complex interplay between the immune system and central nervous system (CNS). Neuroinflammation, once considered a bystander effect of neural injury, is now recognized as a critical driver of numerous neurological disorders, including Alzheimer’s disease, multiple sclerosis, Parkinson’s disease, and psychiatric conditions such as depression and schizophrenia.

This Special Issue brings together original research articles and comprehensive reviews that explore the mechanisms underlying CNS immune activation, the role of glial cells, blood–brain barrier dysfunction, and emerging neuroimmune pathways. Emphasis is placed on novel biomarkers, therapeutic targets, and the translational potential of immunomodulatory strategies. Studies employing advanced techniques such as single-cell sequencing, in vivo imaging, and systems biology contribute to a deeper understanding of the dynamic immune responses within the brain.

By fostering interdisciplinary collaboration across immunology, neuroscience, and clinical research, this Special Issue aims to fill knowledge gaps and promote the development of targeted therapies for neuroinflammatory conditions. Collectively, the contributions offer valuable insights into how immune dysregulation contributes to CNS pathology and how restoring immune balance could transform the treatment of neurological diseases.

Dr. Bojan Shutinoski
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 250 words) can be sent to the Editorial Office for assessment.

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. Brain Sciences is an international peer-reviewed open access monthly 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 2200 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
  • immune response
  • glial cells
  • blood–brain barrier
  • neurodegenerative diseases

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

Published Papers (2 papers)

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Research

35 pages, 25641 KB  
Article
Inhibition of Astrocytic JMJD3 Attenuates Neuroinflammation-Mediated Blood–Brain Barrier Disruption and Improves Functional Recovery After Intracerebral Hemorrhage in Mice
by Quan Zhang, Dewen Ru, Jiang Fang, Jun Zeng, Qiang Yuan, Zhuoying Du, Gang Wu, Jianhong Zhu and Jin Hu
Brain Sci. 2026, 16(5), 454; https://doi.org/10.3390/brainsci16050454 - 24 Apr 2026
Viewed by 199
Abstract
Background: Intracerebral hemorrhage (ICH) is a devastating subtype of stroke, in which neuroinflammation and blood–brain barrier (BBB) disruption are secondary pathophysiological events that drive progressive brain injury. Histone lysine demethylase JMJD3 (Jumonji C domain-containing protein 3) is a master epigenetic switch governing inflammatory [...] Read more.
Background: Intracerebral hemorrhage (ICH) is a devastating subtype of stroke, in which neuroinflammation and blood–brain barrier (BBB) disruption are secondary pathophysiological events that drive progressive brain injury. Histone lysine demethylase JMJD3 (Jumonji C domain-containing protein 3) is a master epigenetic switch governing inflammatory signaling; however, its participation in ICH-induced vascular disruption and its possible mechanism remain elusive. Objective: To examine the expression patterns of JMJD3 in the context of ICH and to evaluate the therapeutic potential of its specific inhibitor, GSK-J4, in attenuating neuroinflammation and BBB disruption in a murine ICH model. Methods: Hemin treatment of a mouse C8-D1A astrocytic cell line was used to develop an in vitro ICH model. The transcript level of the Jmjd3 gene and its correlation with pro-inflammatory signaling were analyzed with or without GSK-J4 pretreatment. ICH in vivo was created experimentally in adult male C57BL/6 mice through stereotactic striatal injection of collagenase IV, and the mice were randomly assigned to sham, ICH + vehicle, and ICH + GSK-J4 (30 mg/kg intraperitoneally (i.p.), every other day starting three days before ICH) groups. At three days post-ICH, ipsilateral brain tissues were collected to detect JMJD3 cellular localization, pro-inflammatory mediator levels, tight junction protein expression, BBB ultrastructure, and hematoma volume. White matter integrity and neuronal recovery were assessed on day 7, and sensorimotor function was assessed longitudinally on days 1, 3, 5, 7, and 14. Results: Jmjd3 gene transcription was upregulated in hemin-treated astrocytes and correlated positively with IL-6 pro-inflammatory signaling activation. In vivo, the co-localization of JMJD3 with the astrocytic identifier glial fibrillary acidic protein (GFAP) was markedly increased in the area adjacent to the hematoma at three days post-ICH. GSK-J4 administration significantly suppressed the pro-inflammatory signaling cascade by decreasing the levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), and matrix metalloproteinase-9 (MMP-9), enhanced brain vascular structural and functional integrity by upregulating tight junction proteins zonula occludens protein-1 (ZO-1) and claudin-5, improved BBB ultrastructural integrity, and decreased hematoma volume at three days post-ICH. Furthermore, GSK-J4 administration promoted white matter integrity (increased myelin basic protein [MBP] expression) and neuronal recovery (increased neuron-specific nuclear protein [NeuN] expression) at seven days post-ICH and significantly improved the performance of ICH mice in sensorimotor behavioral tests. Conclusions: Astrocytic JMJD3 is upregulated following ICH and promotes neuroinflammation, which in turn mediates BBB disruption. Pharmacological inhibition of JMJD3 by GSK-J4 attenuates neuroinflammation and subsequent BBB damage, accelerates hematoma resolution, and promotes histological and functional recovery after ICH, likely by downregulating MMP-9 expression. These findings identify astrocytic JMJD3 as a novel epigenetic therapeutic target for acute ICH. Full article
(This article belongs to the Special Issue Advances in Neuroinflammation and Immune Response)
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16 pages, 1041 KB  
Article
Comprehensive Proteomic Profiling Reveals Dysregulation of Angiogenesis and Inflammatory Pathways in the Brains of SIRT3 Knockout Mice
by Qingping He, Samia Khan, Linlin Wang, Gordon C. Ibeanu and P. Andy Li
Brain Sci. 2026, 16(3), 270; https://doi.org/10.3390/brainsci16030270 - 28 Feb 2026
Viewed by 684
Abstract
Background: Sirtuin 3 (SIRT3), a mitochondrial NAD+-dependent deacetylase, plays a central role in regulating mitochondrial metabolism, oxidative stress, and cell survival. Although SIRT3 has been implicated in angiogenesis, apoptosis, and inflammation, its global proteomic impact on the brain remains unclear. This [...] Read more.
Background: Sirtuin 3 (SIRT3), a mitochondrial NAD+-dependent deacetylase, plays a central role in regulating mitochondrial metabolism, oxidative stress, and cell survival. Although SIRT3 has been implicated in angiogenesis, apoptosis, and inflammation, its global proteomic impact on the brain remains unclear. This study aimed to systematically characterize alterations in angiogenesis-, apoptosis-, chemokine-, and cytokine-related proteins in the brains of SIRT3 knockout (SIRT3 KO aka SIRT3−/−) mice compared with wild-type (WT) controls. Methods: Adult male C57BL/6 WT and SIRT3 KO mice were analyzed using proteome profiler antibody microarrays covering 53 angiogenesis factors, 21 apoptosis markers, 28 chemokines, and 111 cytokines. Protein expression changes were quantified by chemiluminescence imaging and densitometric analysis. Results: The results showed a distinct suppression of angiogenic proteins (amphiregulin, angiogenin, DPPIV, GM-CSF, IGFBP-2, IGFBP-3, IL-1β, PDGF-AA, PDGF-BB, proliferin, serpin F1, thrombospeondin-2, TIMP-4, and VEGF-B), activation of both pro-apoptotic (BAD, cytochrome c, Smac/DIABLO, HIF-1α, Fas, TNF R1, and TRAILR2) and anti-apoptotic, stress-related proteins (Bcl-x, catalase, HO/HMOX2, HSP27, HSP70, and MCL1) in the SIRT3 KO animals compared with the WT controls. Notably, SIRT3 deficiency was associated with increased expression of inflammatory mediators linked to glial activation and neurodegeneration (BLC/CCL13, LIX/CXCL5, MIG/CXCL9, chitinase 3-like 1, CCL22/MDC, IL-6, myeloperoxidase, osteopontin, RBP4, Reg3G, and TNF-α), alongside disturbed proteins involved in immune surveillance and vascular remodeling (6Ckine/CCL21, chemerin, DF, EGF, fractalkine/CX3CL1, HGF, IGFBP-6, IL-16, and I-TAC). Conclusions: Collectively, these findings demonstrate that SIRT3 is a key regulator of mitochondrial-dependent vascular, apoptotic, and neuroimmune pathways in the brain, and that its loss creates a molecular environment consistent with heightened vulnerability to neurodegenerative processes. Full article
(This article belongs to the Special Issue Advances in Neuroinflammation and Immune Response)
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