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Blood-Brain Barrier in Neuroinflammation and Neurological Diseases
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Blood-Brain Barrier in Neuroinflammation and Neurological Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (20 September 2024) | Viewed by 7025

Special Issue Editor

Dr. Fumitaka Shimizu

E-Mail Website
Guest Editor
Department of Neurology and Clinical Neuroscience, Graduate School of Medicine, Yamaguchi University, Ube 755-8505, Japan
Interests: neuroimmune disease; blood-brain barrier; blood-nerve barrier

Special Issue Information

Dear Colleagues,

The blood-brain barrier (BBB) plays a role as a structural and functional barrier that restricts the passage of soluble mediators and leukocytes from the blood to the central nervous system (CNS). Breakdown of the BBB is the key feature in several neuroimmunological diseases, including multiple sclerosis, neuromyelitis optica, collagen disease and autoimmune encephalitis. In addition, dysfunction of BBB is also noted in various neurological diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, trauma, diabetes, hypertension, cerebral small vessel disease and neuropathic pain. However, optimal treatment targeting the BBB has not been yet developed.

This Special Issue aims to focus on both basic molecular science and translational research on the blood-brain barrier in neuroinflammation and neurological diseases. We invite submissions of manuscripts related to the establishment of new BBB in vitro/in vivo models, pathological observation of BBB, or new diagnostic biomarkers of BBB breakdown in these diseases, the blood-nerve barrier and blood–CSF barrier. Review articles on the BBB highlighting the pathomechanisms and treatment strategies in these diseases will also be accepted.

Dr. Fumitaka Shimizu
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • blood-brain barrier
  • in vitro model
  • in vivo model
  • pathology
  • blood–spinal cord barrier
  • blood–CSF barrier
  • blood–nerve barrier
  • multiple sclerosis
  • neuromyelitis optica
  • Alzheimer’s disease
  • Parkinson’s disease
  • collagen disease
  • autoimmune encephalitis
  • amyotrophic lateral sclerosis
  • trauma
  • diabetes
  • cerebral small vessel disease
  • neuropathic pain
  • autoimmune neuropathy

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Published Papers (4 papers)

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Research

13 pages, 2652 KiB  
Article
Expression of Manganese Transporters ZIP8, ZIP14, and ZnT10 in Brain Barrier Tissues
by Shannon Morgan McCabe and Ningning Zhao
Int. J. Mol. Sci. 2024, 25(19), 10342; https://doi.org/10.3390/ijms251910342 - 26 Sep 2024
Viewed by 772
Abstract
Manganese (Mn) is an essential trace mineral for brain function, but excessive accumulation can cause irreversible nervous system damage, highlighting the need for proper Mn balance. ZIP14, ZnT10, and ZIP8 are key transporters involved in maintaining Mn homeostasis, particularly in the absorption and [...] Read more.
Manganese (Mn) is an essential trace mineral for brain function, but excessive accumulation can cause irreversible nervous system damage, highlighting the need for proper Mn balance. ZIP14, ZnT10, and ZIP8 are key transporters involved in maintaining Mn homeostasis, particularly in the absorption and excretion of Mn in the intestine and liver. However, their roles in the brain are less understood. The blood–cerebrospinal fluid barrier and the blood–brain barrier, formed by the choroid plexus and brain blood vessels, respectively, are critical for brain protection and brain metal homeostasis. This study identified ZIP14 on the choroid plexus epithelium, and ZIP8 and ZnT10 in brain microvascular tissue. We show that despite significant Mn accumulation in the CSF of Znt10 knockout mice, ZIP14 expression levels in the blood–cerebrospinal fluid barrier remain unchanged, indicating that ZIP14 does not have a compensatory mechanism for regulating Mn uptake in the brain in vivo. Additionally, Mn still enters the CSF without ZIP14 when systemic levels rise. This indicates that alternative transport mechanisms or compensatory pathways ensure Mn balance in the CSF, shedding light on potential strategies for managing Mn-related disorders. Full article
(This article belongs to the Special Issue Blood-Brain Barrier in Neuroinflammation and Neurological Diseases)
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16 pages, 2517 KiB  
Article
Modeling of Blood–Brain Barrier (BBB) Dysfunction and Immune Cell Migration Using Human BBB-on-a-Chip for Drug Discovery Research
by Masato Ohbuchi, Mayu Shibuta, Kazuhiro Tetsuka, Haruna Sasaki-Iwaoka, Masayo Oishi, Fumitaka Shimizu and Yasuhisa Nagasaka
Int. J. Mol. Sci. 2024, 25(12), 6496; https://doi.org/10.3390/ijms25126496 - 12 Jun 2024
Cited by 2 | Viewed by 2742
Abstract
Blood–brain barrier (BBB) dysfunction is a key feature in neuroimmunological and neurodegenerative diseases. In this study, we developed a microfluidic human BBB-on-a-chip to model barrier dysfunction and immune cell migration using immortalized TY10 brain endothelial cells, pericytes, and astrocytes. It was found that [...] Read more.
Blood–brain barrier (BBB) dysfunction is a key feature in neuroimmunological and neurodegenerative diseases. In this study, we developed a microfluidic human BBB-on-a-chip to model barrier dysfunction and immune cell migration using immortalized TY10 brain endothelial cells, pericytes, and astrocytes. It was found that immortalized TY10 brain endothelial cells developed a microvascular structure under flow. Pericytes were localized on the basal side surrounding the TY10 microvascular structure, showing an in vivo-like structure. Barrier integrity increased under co-culture with pericytes. In addition, both ethylenediaminetetraacetic acid (EDTA) and anti-Claudin-5 (CLDN5) neutralizing antibody caused a decrease in the transendothelial electrical resistance (TEER). EDTA caused the leakage of 20 kDa dextran, suggesting different effects on the BBB based on the mechanism of action, whereas anti-CLDN5 antibody did not cause leakage. In the tri-culture model, human T cells migrated through endothelial vessels towards basal C-X-C motif chemokine ligand 12 (CXCL12). The live-imaging analysis confirmed the extravasation of fluorescence-labelled T cells in a CXCL12-concentration- and time-dependent manner. Our BBB model had an in vivo-like structure and successfully represented barrier dysfunction and transendothelial T cell migration. In addition, our study suggests that the inhibition of CLDN5 attenuates the BBB in humans. This platform has various potential uses in relation to the BBB in both drug discovery research and in elucidating the mechanisms of central nervous system diseases. Full article
(This article belongs to the Special Issue Blood-Brain Barrier in Neuroinflammation and Neurological Diseases)
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15 pages, 5739 KiB  
Article
Anti-HMGB1 mAb Therapy Reduces Epidural Hematoma Injury
by Shangze Gao, Dengli Wang, Keyue Liu, Yasuko Tomono, Li Fu, Yuan Gao, Yohei Takahashi, Mariko Yata and Masahiro Nishibori
Int. J. Mol. Sci. 2024, 25(11), 5889; https://doi.org/10.3390/ijms25115889 - 28 May 2024
Viewed by 1124
Abstract
Epidural and subdural hematomas are commonly associated with traumatic brain injury. While surgical removal is the primary intervention for these hematomas, it is also critical to prevent and reduce complications such as post-traumatic epilepsy, which may result from inflammatory responses in the injured [...] Read more.
Epidural and subdural hematomas are commonly associated with traumatic brain injury. While surgical removal is the primary intervention for these hematomas, it is also critical to prevent and reduce complications such as post-traumatic epilepsy, which may result from inflammatory responses in the injured brain areas. In the present study, we observed that high mobility group box-1 (HMGB1) decreased in the injured brain area beneath the epidural hematoma (EDH) in rats, concurrent with elevated plasma levels of HMGB1. Anti-HMGB1 monoclonal antibody therapy strongly inhibited both HMGB1 release and the subsequent increase in plasma levels. Moreover, this treatment suppressed the up-regulation of inflammatory cytokines and related molecules such as interleukin-1-beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and inducible nitric oxide synthase (iNOS) in the injured areas. Our in vitro experiments using SH-SY5Y demonstrated that hematoma components—thrombin, heme, and ferrous ion— prompted HMGB1 translocation from the nuclei to the cytoplasm, a process inhibited by the addition of the anti-HMGB1 mAb. These findings suggest that anti-HMGB1 mAb treatment not only inhibits HMGB1 translocation but also curtails inflammation in injured areas, thereby protecting the neural tissue. Thus, anti-HMGB1 mAb therapy could serve as a complementary therapy for an EDH before/after surgery. Full article
(This article belongs to the Special Issue Blood-Brain Barrier in Neuroinflammation and Neurological Diseases)
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15 pages, 1932 KiB  
Article
The Blood–Brain Barrier Is Unaffected in the Ndufs4−/− Mouse Model of Leigh Syndrome
by Robin Reynaud-Dulaurier, Romain Clément, Sara Yjjou, Cassandra Cresson, Yasmina Saoudi, Mathilde Faideau and Michael Decressac
Int. J. Mol. Sci. 2024, 25(9), 4828; https://doi.org/10.3390/ijms25094828 - 29 Apr 2024
Viewed by 1445
Abstract
Mitochondrial dysfunction plays a major role in physiological aging and in many pathological conditions. Yet, no study has explored the consequence of primary mitochondrial deficiency on the blood–brain barrier (BBB) structure and function. Addressing this question has major implications for pharmacological and genetic [...] Read more.
Mitochondrial dysfunction plays a major role in physiological aging and in many pathological conditions. Yet, no study has explored the consequence of primary mitochondrial deficiency on the blood–brain barrier (BBB) structure and function. Addressing this question has major implications for pharmacological and genetic strategies aimed at ameliorating the neurological symptoms that are often predominant in patients suffering from these conditions. In this study, we examined the permeability of the BBB in the Ndufs4−/− mouse model of Leigh syndrome (LS). Our results indicated that the structural and functional integrity of the BBB was preserved in this severe model of mitochondrial disease. Our findings suggests that pharmacological or gene therapy strategies targeting the central nervous system in this mouse model and possibly other models of mitochondrial dysfunction require the use of specific tools to bypass the BBB. In addition, they raise the need for testing the integrity of the BBB in complementary in vivo models. Full article
(This article belongs to the Special Issue Blood-Brain Barrier in Neuroinflammation and Neurological Diseases)
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