An intact functioning blood–brain barrier (BBB) is fundamental to proper homoeostatic maintenance and perfusion of the central nervous system (CNS). Inflammatory damage to the unique microvascular endothelial cell monolayer that constitutes the luminal BBB surface, leading to elevated capillary permeability, has been linked to various neurological disorders ranging from ischaemic stroke and traumatic brain injury, to neurodegenerative disease and CNS infections. Moreover, the neuroinflammatory cascade that typically accompanies BBB failure in these circumstances has been strongly linked to elevated levels of pro-inflammatory cytokines such as tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6). This mini review will examine our current knowledge of how cytokines may dysregulate the interendothelial paracellular pathway leading to elevated BBB permeability. The mechanistic role of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase)-induced oxidative stress in these events will also be addressed.
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August 2015
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Review Article|
August 03 2015
The blood–brain barrier endothelium: a target for pro-inflammatory cytokines
Keith D. Rochfort;
Keith D. Rochfort
*School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland
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Philip M. Cummins
Philip M. Cummins
1
*School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland
†Centre for Preventive Medicine, Dublin City University, Glasnevin, Dublin 9, Ireland
1To whom correspondence should be addressed (emailphil.cummins@dcu.ie).
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Publisher: Portland Press Ltd
Received:
December 16 2014
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2015 Authors; published by Portland Press Limited
2015
Biochem Soc Trans (2015) 43 (4): 702–706.
Article history
Received:
December 16 2014
Citation
Keith D. Rochfort, Philip M. Cummins; The blood–brain barrier endothelium: a target for pro-inflammatory cytokines. Biochem Soc Trans 1 August 2015; 43 (4): 702–706. doi: https://doi.org/10.1042/BST20140319
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