Abstract
The brain is protected by a tight barrier between the blood and parenchyma. This so-called blood--brain barrier protects the brain from invading pathogens, infiltrating immune cells, and the extravasation of serum proteins. Beside pericytes and astrocytes mainly endothelial cells form this barrier.
Inflammation leads to an increase in the permeability of the blood–brain barrier. NF-κB is activated during inflammation and is a key regulator of inflammatory processes. In brain endothelial cells NF-κB protects the blood–brain barrier. Loss of the NF-κB activating protein NEMO in brain endothelial cells leads to endothelial cell death, increased permeability, and epilepsy in mice as well as in humans with the hereditary disease incontinentia pigmenti. Therefore, inflammatory mediators are able to disturb but also to protect the blood–brain barrier.
Inflammation leads to an increase in the permeability of the blood–brain barrier. NF-κB is activated during inflammation and is a key regulator of inflammatory processes. In brain endothelial cells NF-κB protects the blood–brain barrier. Loss of the NF-κB activating protein NEMO in brain endothelial cells leads to endothelial cell death, increased permeability, and epilepsy in mice as well as in humans with the hereditary disease incontinentia pigmenti. Therefore, inflammatory mediators are able to disturb but also to protect the blood–brain barrier.
| Original language | English |
|---|---|
| Journal | Neuroforum |
| Volume | 7 |
| Issue number | 2 |
| Pages (from-to) | 23-30 |
| Number of pages | 8 |
| ISSN | 1868-856X |
| DOIs | |
| Publication status | Published - 01.06.2016 |
Research Areas and Centers
- Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)
