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Tight junctions in brain barriers during central nervous system inflammation
Caroline Coisne1, Britta Engelhardt
1Theodor Kocher Institute, University of Bern, Bern, Switzerland. caroline.coisne@tki.unibe.ch
Central nervous system (CNS) homeostasis relies on intact blood-brain barrier (BBB) and blood-cerebrospinal fluid (CSF) barrier (BCSFB). Inflammation disrupts these barriers via tight junction alterations, impacting neurological disorders.
Area of Science:
- Neuroscience
- Cell Biology
- Immunology
Background:
- Central nervous system (CNS) homeostasis is crucial for neuronal function.
- The blood-brain barrier (BBB) and blood-cerebrospinal fluid (CSF) barrier (BCSFB) maintain CNS integrity.
- Tight junctions (TJs) between cells form these physical barriers.
Purpose of the Study:
- To review the cellular and molecular aspects of TJ complexes at the BBB and BCSFB.
- To emphasize the role of CNS inflammation and reactive oxygen species in TJ dysfunction.
- To understand how barrier dysfunction contributes to neurological disorders.
Main Methods:
- Literature review of studies on CNS barriers and inflammation.
- Analysis of TJ protein composition, function, and dynamics.
- Focus on the impact of pro-inflammatory cytokines, matrix metalloproteases, and reactive oxygen species.
Main Results:
- CNS inflammatory disorders alter BBB and BCSFB integrity.
- Pro-inflammatory factors and reactive oxygen species disrupt TJ complexes.
- Barrier dysfunction contributes to neurological disorders through leakage and inflammatory cell migration.
Conclusions:
- Dysfunctional TJs at the BBB and BCSFB are implicated in CNS inflammatory disorders.
- Understanding TJ alterations is key to addressing neurological diseases.
- Reactive oxygen species play a significant role in barrier disruption.
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