Interleukin-1β induces an inflammatory response and the breakdown of the endothelial cell layer in an improved human THBMEC-based in vitro blood–brain barrier model

Cytokine-mediated dysregulation of zonula occludens-1 properties in human brain microvascular endothelium

“…Using the transient middle cerebral artery occlusion (tMCAO) model, researchers have recently demonstrated in vivo how ischemic stroke conditions disrupt ZO-1 expression and localization at the cell-cell border in cerebral microvessels, correlating with barrier failure and extravasation (Huang et al, 2013;Zehendner et al, 2013), an inflammatory process in which multiple cytokines are implicated. Consistent with this notion, the ability of TNF-α to disrupt ZO-1 localization to the cell-cell border in microvascular endothelial cells in vitro for example, has previously been reported (Lutgendorf et al, 2014), whilst other recent microvascular endothelial studies have demonstrated how ZO-1 dysregulation may accompany injury-specific induction of IL-6 (Chaudhuri et al, 2008;Labus et al, 2014). Notwithstanding these observations however, a fuller understanding of the relationship between proinflammatory cytokines and ZO-1 within the BBB microvascular endothelium would complement the existing knowledge base.…”

“…Importantly, some distinctions between our data and other published models are apparent. For example, the lack of effect of 10 ng/ml TNF-α treatment for 24 h on ZO-1 mRNA/protein expression recently reported by Labus et al (2014) using SV-40LT "immortalized" HBMvECs highlights a potentially important dose-sensitivity issue between transformed versus primaryderived cell lines for studies of this kind. Similarly, the observed lack of effect of TNF-α treatment for 24 h on ZO-1 protein expression reported for HUVECs, despite re-distribution of ZO-1 away from tight junctions (McKenzie and Ridley, 2007), may reflect phenotypic differences between microvascular versus macrovascular endothelial cells.…”

Pathogens Penetrating the Central Nervous System: Infection Pathways and the Cellular and Molecular Mechanisms of Invasion

“…In vivo and in vitro studies have shown that group B streptococci, pneumococci, and S. suis induce the production of a range of cytokines and chemokines, including IL-1␤, IL-6, IL-8, IL-10, TNF-␣, macrophage chemoattractant protein 1 (MCP-1), granulocyte-macrophage colony-stimulating factor (GM-CSF), Gro-␣, and Gro-␤, in brain microvascular endothelial cells (109,(256)(257)(258)) and brain tissue (94,259,260). The stimulation of HBMECs with cytokines (including TNF-␣, IL-1␤, IL-6, and IL-17F) leads to cytoskeletal rearrangements and a redistribution of tight junction and adherens junction proteins, resulting in a decrease in barrier integrity (261)(262)(263)(264)(265)(266)(267). Therefore, the host inflammatory response to group B streptococcus, S. pneumoniae, and S. suis meningitis may contribute to the disruption of tight junctions.…”

Purple sweet potato color inhibits endothelial premature senescence by blocking the NLRP3 inflammasome

“…However, the implication of NLRP3 in the onset of atherosclerosis, In addition to IL-1β, endothelial cells can release cytokines including IL-8, a member of the cysteine X cysteine chemokine subfamily, and chemokines such as monocyte chemotactic protein 1 (MCP-1). Moreover, the release of IL-8 and MCP-1 can be promoted by IL-1β [67,68]. Papers have demonstrated that senescent endothelial cells displayed increased expression of IL-8 and MCP-1, and these cytokines mediated senescence and impaired endothelial function [40,69].…”