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The role of the blood–brain barrier during neurological disease and infection

Patabendige, Adjanie, Janigro, Damir·2023·Biochemical Society Transactions
DOI 10.1042/bst20220830PMC PMC10212550
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Abstract

A healthy brain is protected by the blood–brain barrier (BBB), which is formed by the endothelial cells that line brain capillaries. The BBB plays an extremely important role in supporting normal neuronal function by maintaining the homeostasis of the brain microenvironment and restricting pathogen and toxin entry to the brain. Dysfunction of this highly complex and regulated structure can be life threatening. BBB dysfunction is implicated in many neurological diseases such as stroke, Alzheimer's disease, multiple sclerosis, and brain infections. Among other mechanisms, inflammation and/or flow disturbances are major causes of BBB dysfunction in neurological infections and diseases. In particular, in ischaemic stroke, both inflammation and flow disturbances contribute to BBB disruption, leading to devastating consequences. While a transient or minor disruption to the barrier function could be tolerated, chronic or a total breach of the barrier can result in irreversible brain damage. It is worth noting that timing and extent of BBB disruption play an important role in the process of any repair of brain damage and treatment strategies. This review evaluates and summarises some of the latest research on the role of the BBB during neurological disease and infection with a focus on the effects of inflammation and flow disturbances on the BBB. The BBB's crucial role in protecting the brain is also the bottleneck in central nervous system drug development. Therefore, innovative strategies to carry therapeutics across the BBB and novel models to screen drugs, and to study the complex, overlapping mechanisms of BBB disruption are urgently needed.

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Figure 1. Structure of the blood–brain barrier (BBB). The BBB is formed by brain endothelial cells that line cerebral capillaries and is the main protective physiological barrier preventing the entry of toxins and pathogens into the brain. These endothelial cells are supported by other cells such as astrocytes and pericytes of the neurovascular unit, which are important in inducing and maintaining BBB characteristics. Brain endothelial cells differ from those of peripheral tissues by having more complex intercellular tight junctions that restrict the paracellular permeation of molecules through the junctional cleft. Furthermore, endothelial cells in vivo are continuously exposed to shear stress (the frictional force generated by blood flow), which affects endothelial cell structure and function.
Figure 1. Structure of the blood–brain barrier (BBB). The BBB is formed by brain endothelial cells that line cerebral capillaries and is the main protective physiological barrier preventing the entry of toxins and pathogens into the brain. These endothelial cells are supported by other cells such as astrocytes and pericytes of the neurovascular unit, which are important in inducing and maintaining BBB characteristics. Brain endothelial cells differ from those of peripheral tissues by having more complex intercellular tight junctions that restrict the paracellular permeation of molecules through the junctional cleft. Furthermore, endothelial cells in vivo are continuously exposed to shear stress (the frictional force generated by blood flow), which affects endothelial cell structure and function.CC BY · PubMed Central
Figure 2. Blood–brain barrier (BBB) disruption during neurological infections and diseases. BBB disruption is implicated in many neurological infections and diseases, including neurodegenerative diseases, ischaemic stroke as well as viral infections such as SARS-CoV-2, and peripheral diseases such as atrial fibrillation. Disruption of the BBB may involve the opening of tight junctions, damage to the endothelium, increased transport of molecules across the BBB (transcytosis) and alterations in transport systems. Inflammation is a final common pathway in many neurological diseases, allowing immune cell and pathogen entry to the brain, which leaves the brain vulnerable to damage. Furthermore, abnormal flow patterns or flow cessation can lead to changes in shear stress or pulsatility. This can deteriorate the brain endothelium and lead to barrier impairment. Deterioration in neuroprotective BBB function plays a major role in the pathogenesis of disease since the BBB dynamically responds to many events associated with flow disturbances, oxidative stress and proinflammatory cytokine generation. Any condition that affects the functional integrity of the BBB will cause secondary effects on cerebral blood flow and vascular tone, resulting in further damage to the brain.
Figure 2. Blood–brain barrier (BBB) disruption during neurological infections and diseases. BBB disruption is implicated in many neurological infections and diseases, including neurodegenerative diseases, ischaemic stroke as well as viral infections such as SARS-CoV-2, and peripheral diseases such as atrial fibrillation. Disruption of the BBB may involve the opening of tight junctions, damage to the endothelium, increased transport of molecules across the BBB (transcytosis) and alterations in transport systems. Inflammation is a final common pathway in many neurological diseases, allowing immune cell and pathogen entry to the brain, which leaves the brain vulnerable to damage. Furthermore, abnormal flow patterns or flow cessation can lead to changes in shear stress or pulsatility. This can deteriorate the brain endothelium and lead to barrier impairment. Deterioration in neuroprotective BBB function plays a major role in the pathogenesis of disease since the BBB dynamically responds to many events associated with flow disturbances, oxidative stress and proinflammatory cytokine generation. Any condition that affects the functional integrity of the BBB will cause secondary effects on cerebral blood flow and vascular tone, resulting in further damage to the brain.CC BY · PubMed Central

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Sorted by citations

Metadata

Authors
Patabendige, A., & Janigro, D.
Affiliations
  • 1Brain Barriers Research Group, Department of Biology, Edge Hill University, Ormskirk, U.K.
  • 4Flocel Inc., Cleveland, OH, U.S.A.
ORCID
Patabendige, Adjanie
Venue
Biochemical Society Transactions
Publisher
Portland Press Ltd.
Published
2023-03-17
Volume
51
Issue
2
Pages
613-626
ISSN
  • 0300-5127
  • 1470-8752
DOI
10.1042/bst20220830
PMC
PMC10212550
Cited by
112
References
23
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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