Mechanisms of restriction of viral neuroinvasion at the blood–brain barrier

•Neurotropic viruses invade the CNS via several routes including direct transit across the blood–brain barrier (BBB).•Pro-inflammatory cytokines promote BBB breakdown during viral infection.•IFN-β, IFN-λ, and TAM receptor signaling enhance BBB integrity.•Gastrointestinal microbiota modulate BBB func...

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Published inCurrent opinion in immunology Vol. 38; pp. 18 - 23
Main Authors Miner, Jonathan J, Diamond, Michael S
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.02.2016
Subjects
Allergy and Immunology
Animals
Astrocytes - immunology
Astrocytes - pathology
Astrocytes - virology
Blood-Brain Barrier - immunology
Blood-Brain Barrier - pathology
Blood-Brain Barrier - virology
Brain - blood supply
Brain - immunology
Brain - pathology
Brain - virology
Cell Movement
Cytokines - genetics
Cytokines - immunology
Endothelial Cells - immunology
Endothelial Cells - pathology
Endothelial Cells - virology
Gene Expression Regulation
Host-Pathogen Interactions
Humans
Leukocytes - immunology
Leukocytes - pathology
Leukocytes - virology
Microglia - immunology
Microglia - pathology
Microglia - virology
Neurons - immunology
Neurons - pathology
Neurons - virology
Pericytes - immunology
Pericytes - pathology
Pericytes - virology
Signal Transduction
Virus Diseases - immunology
Virus Diseases - pathology
Virus Diseases - virology
Viruses - immunology
Viruses - pathogenicity
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Abstract •Neurotropic viruses invade the CNS via several routes including direct transit across the blood–brain barrier (BBB).•Pro-inflammatory cytokines promote BBB breakdown during viral infection.•IFN-β, IFN-λ, and TAM receptor signaling enhance BBB integrity.•Gastrointestinal microbiota modulate BBB function. The blood–brain barrier (BBB) consists of highly specialized cells including brain microvascular endothelial cells, astrocytes, microglia, pericytes, and neurons, which act in concert to restrict the entry of pathogens, immune cells, and soluble molecules into the central nervous system (CNS). If pathogens manage to cross the BBB and establish infection within the CNS, the BBB can open in a regulated manner to allow leukocyte transmigration into the CNS so that microbes, infected cells, and debris can be cleared. This review highlights how different inflammatory cytokines or signaling pathways disrupt or enhance BBB integrity in a way that regulates entry of neurotropic viruses into the CNS.
AbstractList The blood-brain barrier (BBB) consists of highly specialized cells including brain microvascular endothelial cells, astrocytes, microglia, pericytes, and neurons, which act in concert to restrict the entry of pathogens, immune cells, and soluble molecules into the central nervous system (CNS). If pathogens manage to cross the BBB and establish infection within the CNS, the BBB can open in a regulated manner to allow leukocyte transmigration into the CNS so that microbes, infected cells, and debris can be cleared. This review highlights how different inflammatory cytokines or signaling pathways disrupt or enhance BBB integrity in a way that regulates entry of neurotropic viruses into the CNS.
The blood-brain barrier (BBB) consists of highly specialized cells including brain microvascular endothelial cells, astrocytes, microglia, pericytes, and neurons, which act in concert to restrict the entry of pathogens, immune cells, and soluble molecules into the central nervous system (CNS). If pathogens manage to cross the BBB and establish infection within the CNS, the BBB can open in a regulated manner to allow leukocyte transmigration into the CNS so that microbes, infected cells, and debris can be cleared. This review highlights how different inflammatory cytokines or signaling pathways disrupt or enhance BBB integrity in a way that regulates entry of neurotropic viruses into the CNS.The blood-brain barrier (BBB) consists of highly specialized cells including brain microvascular endothelial cells, astrocytes, microglia, pericytes, and neurons, which act in concert to restrict the entry of pathogens, immune cells, and soluble molecules into the central nervous system (CNS). If pathogens manage to cross the BBB and establish infection within the CNS, the BBB can open in a regulated manner to allow leukocyte transmigration into the CNS so that microbes, infected cells, and debris can be cleared. This review highlights how different inflammatory cytokines or signaling pathways disrupt or enhance BBB integrity in a way that regulates entry of neurotropic viruses into the CNS.
•Neurotropic viruses invade the CNS via several routes including direct transit across the blood–brain barrier (BBB).•Pro-inflammatory cytokines promote BBB breakdown during viral infection.•IFN-β, IFN-λ, and TAM receptor signaling enhance BBB integrity.•Gastrointestinal microbiota modulate BBB function. The blood–brain barrier (BBB) consists of highly specialized cells including brain microvascular endothelial cells, astrocytes, microglia, pericytes, and neurons, which act in concert to restrict the entry of pathogens, immune cells, and soluble molecules into the central nervous system (CNS). If pathogens manage to cross the BBB and establish infection within the CNS, the BBB can open in a regulated manner to allow leukocyte transmigration into the CNS so that microbes, infected cells, and debris can be cleared. This review highlights how different inflammatory cytokines or signaling pathways disrupt or enhance BBB integrity in a way that regulates entry of neurotropic viruses into the CNS.
Highlights • Neurotropic viruses invade the CNS via several routes including direct transit across the blood–brain barrier (BBB). • Pro-inflammatory cytokines promote BBB breakdown during viral infection. • IFN-β, IFN-λ, and TAM receptor signaling enhance BBB integrity. • Gastrointestinal microbiota modulate BBB function.
• Neurotropic viruses invade the CNS via several routes including direct transit across the blood–brain barrier (BBB). • Pro-inflammatory cytokines promote BBB breakdown during viral infection. • IFN-β, IFN-λ, and TAM receptor signaling enhance BBB integrity. • Gastrointestinal microbiota modulate BBB function. The blood–brain barrier (BBB) consists of highly specialized cells including brain microvascular endothelial cells, astrocytes, microglia, pericytes, and neurons, which act in concert to restrict the entry of pathogens, immune cells, and soluble molecules into the central nervous system (CNS). If pathogens manage to cross the BBB and establish infection within the CNS, the BBB can open in a regulated manner to allow leukocyte transmigration into the CNS so that microbes, infected cells, and debris can be cleared. This review highlights how different inflammatory cytokines or signaling pathways disrupt or enhance BBB integrity in a way that regulates entry of neurotropic viruses into the CNS.
Author Diamond, Michael S
Miner, Jonathan J
AuthorAffiliation 2 Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO 63110, USA
1 Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
3 Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO 63110, USA
4 Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St Louis, MO 63110, USA
AuthorAffiliation_xml – name: 2 Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO 63110, USA
– name: 1 Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
– name: 4 Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St Louis, MO 63110, USA
– name: 3 Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO 63110, USA
Author_xml – sequence: 1
  givenname: Jonathan J
  surname: Miner
  fullname: Miner, Jonathan J
  organization: Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
– sequence: 2
  givenname: Michael S
  surname: Diamond
  fullname: Diamond, Michael S
  email: diamond@borcim.wustl.edu
  organization: Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/26590675$$D View this record in MEDLINE/PubMed
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Snippet •Neurotropic viruses invade the CNS via several routes including direct transit across the blood–brain barrier (BBB).•Pro-inflammatory cytokines promote BBB...
Highlights • Neurotropic viruses invade the CNS via several routes including direct transit across the blood–brain barrier (BBB). • Pro-inflammatory cytokines...
The blood-brain barrier (BBB) consists of highly specialized cells including brain microvascular endothelial cells, astrocytes, microglia, pericytes, and...
• Neurotropic viruses invade the CNS via several routes including direct transit across the blood–brain barrier (BBB). • Pro-inflammatory cytokines promote BBB...
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SubjectTerms Allergy and Immunology
Animals
Astrocytes - immunology
Astrocytes - pathology
Astrocytes - virology
Blood-Brain Barrier - immunology
Blood-Brain Barrier - pathology
Blood-Brain Barrier - virology
Brain - blood supply
Brain - immunology
Brain - pathology
Brain - virology
Cell Movement
Cytokines - genetics
Cytokines - immunology
Endothelial Cells - immunology
Endothelial Cells - pathology
Endothelial Cells - virology
Gene Expression Regulation
Host-Pathogen Interactions
Humans
Leukocytes - immunology
Leukocytes - pathology
Leukocytes - virology
Microglia - immunology
Microglia - pathology
Microglia - virology
Neurons - immunology
Neurons - pathology
Neurons - virology
Pericytes - immunology
Pericytes - pathology
Pericytes - virology
Signal Transduction
Virus Diseases - immunology
Virus Diseases - pathology
Virus Diseases - virology
Viruses - immunology
Viruses - pathogenicity
Title Mechanisms of restriction of viral neuroinvasion at the blood–brain barrier
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0952791515001454
https://www.clinicalkey.es/playcontent/1-s2.0-S0952791515001454
https://dx.doi.org/10.1016/j.coi.2015.10.008
https://www.ncbi.nlm.nih.gov/pubmed/26590675
https://www.proquest.com/docview/1760864740
https://www.proquest.com/docview/1762360050
https://pubmed.ncbi.nlm.nih.gov/PMC4715944
Volume 38
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