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Molecular Advances in Blood–Brain Barrier, Blood–Cerebrospinal Fluid Barrier and Cerebrospinal Fluid–Brain Barriers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 December 2024) | Viewed by 2854

Special Issue Editor

Dr. Eva M. Medina-Rodríguez

E-Mail Website
Guest Editor
1. Psychiatry Service, Dr. Peset Hospital (FISABIO), 46020 Valencia, Spain
2. Institute of Agrochemistry and Food Technology (IATA), Spanish National Research Council (CSIC), 46980 Paterna, Spain
Interests: blood-brain barrier; blood-cerebrospinal fluid barrier; CSF-brain barriers

Special Issue Information

Dear Colleagues,

The blood–brain barrier (BBB), blood–cerebrospinal fluid (CSF) barrier (BCSFB), and CSF–brain barriers (CSFBBs) regulate the transport of fluids between the central nervous system and the circulating blood or CSF in order to avoid non-selective crossing of ions, molecules, toxins, and cells into the central nervous system. They are composed of endothelial or epithelial cells, connected by tight junctions, which interact with pericytes and astrocytes in their close vicinity. These barriers are highly selective and their disruption may cause numerous diseases such as stroke, multiple sclerosis, or mental disorders. Disruption of these barriers can be triggered by many factors such as hypoxia, inflammation, or intestinal dysbiosis. The knowledge of the mechanisms that maintain or disrupt these barriers as well as the mechanisms that can repair them is critical to maintaining CNS homeostasis and avoid or treat neurologic diseases.

We are pleased to invite you to contribute with your knowledge and research about the BBB, BCSFB and CSFBBs.

This Special Issue aims to collect cutting-edge information on this topic.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: neuroscience, microbiology, immunology, or clinical research with molecular data.

I look forward to receiving your contributions.

Dr. Eva M. Medina-Rodríguez
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 (BBB)
  • blood–cerebrospinal fluid (CSF) barrier (BCSFB)
  • CSF–brain barriers (CSFBB)
  • brain homeostasis
  • neuroscience
  • depression
  • multiple sclerosis
  • stroke

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Published Papers (3 papers)

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Research

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27 pages, 5835 KiB  
Article
The Factors Associated with the Blood–Brain Barrier Dysfunction in Tick-Borne Encephalitis
by Sambor Grygorczuk, Piotr Czupryna, Diana Martonik, Justyna Adamczuk, Anna Parfieniuk-Kowerda, Anna Grzeszczuk, Wioletta Pawlak-Zalewska, Justyna Dunaj-Małyszko, Kaja Mielczak, Miłosz Parczewski and Anna Moniuszko-Malinowska
Int. J. Mol. Sci. 2025, 26(4), 1503; https://doi.org/10.3390/ijms26041503 - 11 Feb 2025
Viewed by 593
Abstract
The pathogenesis of the central nervous system (CNS) pathology in tick-borne encephalitis (TBE) remains unclear. We attempted to identify mediators of the blood–brain barrier (BBB) disruption in human TBE in paired serum and cerebrospinal fluid (CSF) samples from 100 TBE patients. CSF albumin [...] Read more.
The pathogenesis of the central nervous system (CNS) pathology in tick-borne encephalitis (TBE) remains unclear. We attempted to identify mediators of the blood–brain barrier (BBB) disruption in human TBE in paired serum and cerebrospinal fluid (CSF) samples from 100 TBE patients. CSF albumin quotient (Qalb) was calculated as a measure of BBB impairment. Concentrations of cytokines, cytokine antagonists, adhesion molecules, selectins and matrix metalloproteinases (MMP) were measured with a multiplex bead assay. Single nucleotide polymorphisms (SNP) in genes MIF, TNF, TNFRSF1A, TNFRSF1B, IL-10, TLR3 and TLR4 were studied in patient blood DNA extracts and analyzed for associations with Qalb and/or cytokine concentrations. The multivariate regression models of Qalb were built with the soluble mediators as independent variables. The best models obtained included L-selectin, P-selectin, sVCAM, MMP7, MMP8 (or MMP9) and IL-28A as positive and IL-12p70, IL-15, IL-6Rα/IL-6 ratio and TNF-RII/TNFα ratio as negative correlates of Qalb. The genotype did not associate with Qalb, but polymorphism rs4149570 (in TNFRSF1A) associated with TNFα and rs1800629 (TNF) with MIF concentration. We confirm the association of the TNFα-dependent response, L-selectin and MMP8/MMP9 with BBB disruption and identify its novel correlates (IL-12, IL-15, IL-28A, MMP7). We detect no genotype associations with BBB function in TBE. Full article
(This article belongs to the Special Issue Molecular Advances in Blood–Brain Barrier, Blood–Cerebrospinal Fluid Barrier and Cerebrospinal Fluid–Brain Barriers)
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9 pages, 537 KiB  
Article
Association of Baseline Lipopolysaccharide-Binding Protein with Expanded Disability Status Score Dynamics in Patients with Relapsing–Remitting Multiple Sclerosis: A Pilot Study
by Anda Vilmane, Oksana Kolesova, Zaiga Nora-Krukle, Aleksandrs Kolesovs, Daina Pastare, Liga Jaunozolina, Linda Kande, Jelena Egle, Daniela Kromane, Madara Micule, Sintija Liepina, Estere Zeltina, Sabine Gravelsina, Santa Rasa-Dzelzkaleja, Ludmila Viksna and Guntis Karelis
Int. J. Mol. Sci. 2025, 26(1), 298; https://doi.org/10.3390/ijms26010298 - 31 Dec 2024
Viewed by 706
Abstract
Forecasting the progression of the disease in the early inflammatory stage of the most prevalent type of multiple sclerosis (MS), referred to as relapsing–remitting multiple sclerosis (RRMS), is essential for making prompt treatment modifications, aimed to reduce clinical relapses and disability. In total, [...] Read more.
Forecasting the progression of the disease in the early inflammatory stage of the most prevalent type of multiple sclerosis (MS), referred to as relapsing–remitting multiple sclerosis (RRMS), is essential for making prompt treatment modifications, aimed to reduce clinical relapses and disability. In total, 58 patients with RRMS, having an Expanded Disability Status Scale (EDSS) score less than 4, were included in this study. Baseline magnetic resonance imaging (MRI) was performed, and brain and spinal cord lesions were evaluated. The disability of the patients was evaluated using EDSS at baseline and follow-up; enzyme-linked immunosorbent assays (ELISAs) were also used to determine the level of blood-based inflammation markers in plasma at baseline. The main results demonstrated that the baseline level of LBP was correlated with an increase in EDSS in a short (8–10 months) follow-up period. Furthermore, the prognostic significance of LBP was only observed in patients who received disease-modifying treatment (DMT) before the study. Our results suggest that the baseline level of LBP may be among the predictors of disability progression in RRMS over short follow-up periods, particularly in those receiving treatment. It highlights the effect of endotoxins in the pathogenesis of RRMS. Full article
(This article belongs to the Special Issue Molecular Advances in Blood–Brain Barrier, Blood–Cerebrospinal Fluid Barrier and Cerebrospinal Fluid–Brain Barriers)
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Review

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27 pages, 1397 KiB  
Review
Regulatory T Cell- and Natural Killer Cell-Mediated Inflammation, Cerebral Vasospasm, and Delayed Cerebral Ischemia in Aneurysmal Subarachnoid Hemorrhage—A Systematic Review and Meta-Analysis Approach
by Andreas Pfnür, Benjamin Mayer, Lena Dörfer, Hayrettin Tumani, Daniel Spitzer, Markus Huber-Lang and Thomas Kapapa
Int. J. Mol. Sci. 2025, 26(3), 1276; https://doi.org/10.3390/ijms26031276 - 1 Feb 2025
Cited by 2 | Viewed by 989
Abstract
Aneurysmal subarachnoid hemorrhage (SAH) involves a significant influx of blood into the cerebrospinal fluid, representing a severe form of stroke. Despite advancements in aneurysm closure and neuro-intensive care, outcomes remain impaired due to cerebral vasospasm and delayed cerebral ischemia (DCI). Previous pharmacological therapies [...] Read more.
Aneurysmal subarachnoid hemorrhage (SAH) involves a significant influx of blood into the cerebrospinal fluid, representing a severe form of stroke. Despite advancements in aneurysm closure and neuro-intensive care, outcomes remain impaired due to cerebral vasospasm and delayed cerebral ischemia (DCI). Previous pharmacological therapies have not successfully reduced DCI while improving overall outcomes. As a result, significant efforts are underway to better understand the cellular and molecular mechanisms involved. This review focuses on the activation and effects of immune cells after SAH and their interactions with neurotoxic and vasoactive substances as well as inflammatory mediators. Particular attention is given to clinical studies highlighting the roles of natural killer (NK) cells and regulatory T cells (Treg) cells. Alongside microglia, astrocytes, and oligodendrocytes, NK cells and Treg cells are key contributors to the inflammatory cascade following SAH. Their involvement in modulating the neuro-inflammatory response, vasospasm, and DCI underscores their potential as therapeutic targets and prognostic markers in the post-SAH recovery process. We conducted a systematic review on T cell- and natural killer cell-mediated inflammation and their roles in cerebral vasospasm and delayed cerebral ischemia. We conducted a meta-analysis to evaluate outcomes and mortality in studies focused on NK cell- and T cell-mediated mechanisms. Full article
(This article belongs to the Special Issue Molecular Advances in Blood–Brain Barrier, Blood–Cerebrospinal Fluid Barrier and Cerebrospinal Fluid–Brain Barriers)
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