ArticleInternational journal of molecular sciences2022
TNF-α and IL-1β Modulate Blood-Brain Barrier Permeability and Decrease Amyloid-β Peptide Efflux in a Human Blood-Brain Barrier Model.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.
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Who cites it
112 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.
- Association Between Inflammatory Markers and Cognitive Function in Adults With Bipolar Disorder: A Systematic Review.Acta psychiatrica Scandinavica · 2026Pooled it
- A synopsis of competence-regulated virulence inVirulence · 2026Review
- Review
- The Impact of Overtraining on Anxiety-Like Behavior and Tight Junction Proteins of the Blood-Brain Barrier in Mice.Brain and behavior · 2026Article
- Soluble TREM2 Mediates Blood Brain Barrier Permeability through Astrocyte Reactivity.Research square · 2026Article
- Heart Meets Brain: Insights into Neurocardiac Pathophysiology.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Article
- IL-1β pathway-dependent regulation of glutamate receptor activity by gut microbiota in bipolar depression.Journal of Zhejiang University. Science. B · 2026Article
- Establishment and Optimization of a Human Flow-Based Hollow FiberPharmaceutics · 2026Article
- A Four-Channel Microfluidic Vascular-Wall Chip for Modeling Early Atherosclerosis-Related Endothelial Dysfunction and Evaluating Combined Anti-Inflammatory Treatment.Micromachines · 2026Article
- Importance of the inflammasome in gut-brain axis: from pathological driver to therapeutic target.Inflammopharmacology · 2026Review
- Mechanistically informed circulating biomarkers are associated with acquired epilepsy after neonatal brain injury.Journal of neuroinflammation · 2026Observational
- Malathion-induced neurological alterations associated with dysregulation of RORγt/STAT3/IL-17 and FOXP3/STAT5/IL-10 pathways: potential neuroprotective effects of BCG.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Neurovascular and synaptic milieu of brain-resident cells in cognitive dysfunction of myalgic encephalomyelitis/chronic fatigue syndrome.Journal of translational medicine · 2026Review
- <p>Harnessing MSC‑derived exosomes to modulate the pathophysiology of ASD: Recent advances and therapeutic implications (Review)</p>.International journal of molecular medicine · 2026Review
- The spleen-brain axis in Alzheimer's disease and related dementias: Integrating immune and metabolic regulation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Review
- Consequences of irradiation on blood-brain tumor barrier model of Diffuse Midline Glioma: characterization of physical and metabolic properties.Fluids and barriers of the CNS · 2026Article
- Reframing brain aging: neuroinflammation as an interconnected network process.Frontiers in aging · 2026Review
- Neuroinflammatory mechanisms and pharmacological advances in autism spectrum disorder: from inflammatory pathways to targeted interventions.Frontiers in immunology · 2026Review
52 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
The blood-brain barrier (BBB) is a selective barrier and a functional gatekeeper for the central nervous system (CNS), essential for maintaining brain homeostasis. The BBB is composed of specialized brain endothelial cells (BECs) lining the brain capillaries. The tight junctions formed by BECs regulate paracellular transport, whereas transcellular transport is regulated by specialized transporters, pumps and receptors. Cytokine-induced neuroinflammation, such as the tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), appear to play a role in BBB dysfunction and contribute to the progression of Alzheimer's disease (AD) by contributing to amyloid-β (Aβ) peptide accumulation. Here, we investigated whether TNF-α and IL-1β modulate the permeability of the BBB and alter Aβ peptide transport across BECs. We used a human BBB in vitro model based on the use of brain-like endothelial cells (BLECs) obtained from endothelial cells derived from CD34+ stem cells cocultivated with brain pericytes. We demonstrated that TNF-α and IL-1β differentially induced changes in BLECs' permeability by inducing alterations in the organization of junctional complexes as well as in transcelluar trafficking. Further, TNF-α and IL-1β act directly on BLECs by decreasing LRP1 and BCRP protein expression as well as the specific efflux of Aβ peptide. These results provide mechanisms by which CNS inflammation might modulate BBB permeability and promote Aβ peptide accumulation. A future therapeutic intervention targeting vascular inflammation at the BBB may have the therapeutic potential to slow down the progression of AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.