Blood-Brain Barrier Disruption Induced by Chronic Sleep Loss: Low-Grade Inflammation May Be the Link
Table 2
Inflammatory mediators released during sleep loss that may potentially regulate blood-brain barrier integrity.
Inflammatory mediator
General changes during sleep loss
General effects on blood-brain barrier
TNF-α
circulating levels in human and rodents [29–32] mRNA expression in mice brain [33]
blood-brain barrier permeability in in vivo and in vitro models (rodent and human brain endothelial cells) [38–40] efflux of albumin from brain to blood [43] ZO-1 expression [103] MMP-9 protein expression [106]
IL-1β
circulating levels in human and rodents [3, 4, 29, 49] mRNA expression in mice brain [45]
blood-brain barrier permeability in in vivo and in vitro models (rodent and human brain endothelial cells) [42, 54] TEER of primary cultures of brain endothelial cells and human brain endothelial cells [42, 54] production of PGE and COX [57] ZO-1 expression [103]
IL-6
circulating levels in human after chronic sleep loss [64, 65] circulating levels in humans [62] circulating levels during sleep recovery in humans [69] mRNA expression in human PBMC [50, 67]
TEER in cerebrovascular endothelial cells from rats at higher doses but not at lower doses [42] blood-brain barrier permeability in ischemic brain in rodents [71]
IL-17A
circulating levels in rodents [29] mRNA expression in human PBMC [50]
blood-brain barrier permeability in in vivo and in vitro models (rodent and human brain endothelial cells) [78, 79]
CRP
circulating levels in humans and rodents [4, 8, 50, 67, 81–83]
blood-brain barrier permeability in in vivo and in vitro models (rodent and human brain endothelial cells) [85] ROS production in brain endothelial cells [86]
