title: The blood-brain barrier endothelium: a target for pro-inflammatory cytokines.
abstract: 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.
authors.affiliation: School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland.
authors.forename: Keith D
authors.initials: KD
authors.lastname: Rochfort
authors.affiliation: School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland Centre for Preventive Medicine, Dublin City University, Glasnevin, Dublin 9, Ireland phil.cummins@dcu.ie.
authors.forename: Philip M
authors.initials: PM
authors.lastname: Cummins
mesh_terms: D001812:Blood-Brain Barrier / Q000276:immunology*; D002490:Central Nervous System / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D042783:Endothelial Cells / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D019255:NADPH Oxidases / Q000378:metabolism; D018384:Oxidative Stress
chemical_list: D016207:Cytokines; D019255:NADPH Oxidases
keywords: NADPH oxidase; blood–brain barrier; endothelial; interleukin-6 (IL-6); neuroinflammation; tumour necrosis factor-α (TNF-α)