ArticlePloS one2020
Purified IgG from aquaporin-4 neuromyelitis optica spectrum disorder patients alters blood-brain barrier permeability.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- The IL-1β-STING Signaling Axis Drives Neuromyelitis Optica Pathogenesis in a Murine Model.Annals of neurology · 2026Article
- Neuromyelitis optica spectrum disorder overlapping with Sjögren's disease: immunopathological links and therapeutic implications.Frontiers in immunology · 2026Review
- CSF estrogens' relationships to neuroinflammatory markers and brain networks in middle-aged and older black and white women.Journal of neuroinflammation · 2025Article
- Aquaporin-4 Peptide Injection in Mice Induces Retinal and Optic Nerve Alterations That Simulate Those of Neuromyelitis Optica Spectrum Disorder.Translational vision science & technology · 2025Article
- Article
- The Involvement of Glial Cells in Blood-Brain Barrier Damage in Neuroimmune Diseases.International journal of molecular sciences · 2024Review
- NMOSD IgG Impact Retinal Cells in Murine Retinal Explants.Current issues in molecular biology · 2023Article
- Ependyma: a new target for autoantibodies in neuromyelitis optica?Brain communications · 2022Article
- The Role of Exposomes in the Pathophysiology of Autoimmune Diseases I: Toxic Chemicals and Food.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Review
- Hope for patients with neuromyelitis optica spectrum disorders - from mechanisms to trials.Nature reviews. Neurology · 2021Review
- Treatment of Neuromyelitis Optica Spectrum Disorders.International journal of molecular sciences · 2021Review
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuromyelitis optica spectrum disorders (NMOSD) is a primary astrocytopathy driven by antibodies directed against the aquaporin-4 water channel located at the end-feet of the astrocyte. Although blood-brain barrier (BBB) breakdown is considered one of the key steps for the development and lesion formation, little is known about the molecular mechanisms involved. The aim of the study was to evaluate the effect of human immunoglobulins from NMOSD patients (NMO-IgG) on BBB properties.
methodsFreshly isolated brain microvessels (IBMs) from rat brains were used as a study model. At first, analysis of the secretome profile from IBMs exposed to purified NMO-IgG, to healthy donor IgG (Control-IgG), or non-treated, was performed. Second, tight junction (TJ) proteins expression in fresh IBMs and primary cultures of brain microvascular endothelial cells (BMEC) was analysed by Western blotting (Wb) after exposition to NMO-IgG and Control-IgG. Finally, functional BBB properties were investigated evaluating the presence of rat-IgG in tissue lysate from brain using Wb in the rat-model, and the passage of NMO-IgG and sucrose in a bicameral model.
resultsWe found that NMO-IgG induces functional and morphological BBB changes, including: 1) increase of pro-inflammatory cytokines production (CXCL-10 [IP-10], IL-6, IL-1RA, IL-1β and CXCL-3) in IBMs when exposed to NMO-IgG; 2) decrease of Claudin-5 levels by 25.6% after treatment of fresh IBMs by NMO-IgG compared to Control-IgG (p = 0.002), and similarly, decrease of Claudin-5 by at least 20% when BMEC were cultured with NMO-IgG from five different patients; 3) a higher level of rat-IgG accumulated in periventricular regions of NMO-rats compared to Control-rats and an increase in the permeability of BBB after NMO-IgG treatment in the bicameral model.
conclusionHuman NMO-IgG induces both structural and functional alterations of BBB properties, suggesting a direct role of NMO-IgG on modulation of BBB permeability in NMOSD.
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