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TNF-α and IL-1β Modulate Blood-Brain Barrier Permeability and Decrease Amyloid-β Peptide Efflux in a Human
Romain Versele1,2, Emmanuel Sevin1, Fabien Gosselet1
1Laboratoire de la Barrière Hémato-Encéphalique (LBHE), UR 2465, Université d'Artois, F-62300 Lens, France.
International Journal of Molecular Sciences
|September 23, 2022
Summary
Neuroinflammation from TNF-α and IL-1β increases blood-brain barrier permeability and reduces amyloid-β clearance, potentially worsening Alzheimer
Area of Science:
- Neuroscience
- Cell Biology
- Vascular Biology
Background:
- The blood-brain barrier (BBB) protects the central nervous system (CNS) and is crucial for brain homeostasis.
- BBB dysfunction, linked to neuroinflammation, may drive Alzheimer's disease (AD) progression by increasing amyloid-β (Aβ) accumulation.
Purpose of the Study:
- To investigate how tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) affect BBB permeability and Aβ peptide transport.
- To elucidate mechanisms linking CNS inflammation to BBB dysfunction and Aβ peptide accumulation in AD.
Main Methods:
- Utilized a human in vitro blood-brain barrier model using brain-like endothelial cells (BLECs) cocultivated with brain pericytes.
- Assessed the impact of TNF-α and IL-1β on BLEC permeability, junctional complex organization, and transcellular trafficking.
Main Results:
- TNF-α and IL-1β differentially altered BLEC permeability by affecting junctional complexes and transcellular transport.
- These cytokines reduced LRP1 and BCRP protein expression in BLECs, impairing Aβ peptide efflux.
Conclusions:
- CNS inflammation, mediated by TNF-α and IL-1β, directly impacts BBB integrity and function.
- Targeting vascular inflammation at the BBB may offer a therapeutic strategy to slow Alzheimer's disease progression.
