Inflammatory Mediators and the Blood-Brain Barrier

Author(s):  
Katerina Dorovini-Zis ◽  
Alexander Easton
2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Fanwei Meng ◽  
Lifen Yao

Abstract Epilepsy is a chronic neurological disorder that has an extensive impact on a patient’s life. Accumulating evidence has suggested that inflammation participates in the progression of spontaneous and recurrent seizures. Pro-convulsant incidences can stimulate immune cells, augment the release of pro-inflammatory cytokines, elicit neuronal excitation as well as blood-brain barrier (BBB) dysfunction, and finally trigger the generation or recurrence of seizures. Understanding the pathogenic roles of inflammatory mediators, including inflammatory cytokines, cells, and BBB, in epileptogenesis will be beneficial for the treatment of epilepsy. In this systematic review, we performed a literature search on the PubMed database using the following keywords: “epilepsy” or “seizures” or “epileptogenesis”, and “immunity” or “inflammation” or “neuroinflammation” or “damage-associated molecular patterns” or “cytokines” or “chemokines” or “adhesion molecules” or “microglia” or “astrocyte” or “blood-brain barrier”. We summarized the classic inflammatory mediators and their pathogenic effects in the pathogenesis of epilepsy, based on the most recent findings from both human and animal model studies.


2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
G. Hurtado-Alvarado ◽  
E. Domínguez-Salazar ◽  
L. Pavon ◽  
J. Velázquez-Moctezuma ◽  
B. Gómez-González

Sleep is a vital phenomenon related to immunomodulation at the central and peripheral level. Sleep deficient in duration and/or quality is a common problem in the modern society and is considered a risk factor to develop neurodegenerative diseases. Sleep loss in rodents induces blood-brain barrier disruption and the underlying mechanism is still unknown. Several reports indicate that sleep loss induces a systemic low-grade inflammation characterized by the release of several molecules, such as cytokines, chemokines, and acute-phase proteins; all of them may promote changes in cellular components of the blood-brain barrier, particularly on brain endothelial cells. In the present review we discuss the role of inflammatory mediators that increase during sleep loss and their association with general disturbances in peripheral endothelium and epithelium and how those inflammatory mediators may alter the blood-brain barrier. Finally, this manuscript proposes a hypothetical mechanism by which sleep loss may induce blood-brain barrier disruption, emphasizing the regulatory effect of inflammatory molecules on tight junction proteins.


2019 ◽  
Vol 124 ◽  
pp. 61-66 ◽  
Author(s):  
Shinya Dohgu ◽  
Fuyuko Takata ◽  
Junichi Matsumoto ◽  
Ikuya Kimura ◽  
Atsushi Yamauchi ◽  
...  

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