Infectious immunity in the central nervous system and brain function

Klein, Robyn S; Garber, Charise; Howard, Nicole

doi:10.1038/ni.3656

Cited by 235Neuroinflammation and Neurodegeneration MechanismsInfectious Encephalopathies and EncephalitisTryptophan and brain disorders

Infectious immunity in the central nervous system and brain function

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Klein, Robyn S, Garber, Charise, Howard, Nicole·2017·Nature Immunology

DOI 10.1038/ni.3656PMC PMC5815515

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Abstract

Inflammation is emerging as a critical mechanism underlying neurological disorders of various etiologies, yet its role in altering brain function as a consequence of neuroinfectious disease remains unclear. Although acute alterations in mental status due to inflammation are a hallmark of central nervous system (CNS) infections with neurotropic pathogens, post-infectious neurologic dysfunction has traditionally been attributed to irreversible damage caused by the pathogens themselves. More recently, studies indicate that pathogen eradication within the CNS may require immune responses that interfere with neural cell function and communication without affecting their survival. In this Review we explore inflammatory processes underlying neurological impairments caused by CNS infection and discuss their potential links to established mechanisms of psychiatric and neurodegenerative diseases.

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A handful of viruses, including poliovirus, adenovirus, Epstein-Barr virus (EBV), and West Nile virus, can directly infect human brain endothelial cells by targeting junctional proteins such as JAM-A or transporters such as GLUT1 as entry receptors to get access to the CNS.
“A handful of viruses, including poliovirus, adenovirus, Epstein-Barr virus (EBV), and West Nile virus, can directly infect human brain endothelial cells by targeting junctional proteins such as JAM-Aortransporters such as GLUT1 as entry receptors to get access to the CNS (320).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [320]
The sections on parenchymal infection and CNS anatomy describe West Nile virus as a cause of CNS infection and discuss routes by which pathogens cross the blood–brain barrier (pages not provided). They do not say that the four named viruses directly infect human brain endothelial cells or use JAM-A or GLUT1 as entry receptors; searches for those receptor names and the named viruses did not establish that mechanism. (LLM, conf=0.83)
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Nervous system damage caused by viral infection may be mediated by the immune system.
“Nervous system damage caused by viral infection may be mediated by the immune system (Klein et al., 2017).”
From Nervous system involvement after infection with COVID-19 and other coronaviruses (2020) · cites this paper as Klein et al., 2017

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Blood-Brain Barrier: From Physiology to Disease and Back
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“, IL-1 , IL-6, TNF- , and IFN- ) can be observed across multiple brain regions, including the hippocampus (Howe et al., 2012; Elmore et al., 2014; Heneka et al., 2014; Klein et al., 2017).”
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MicroRNAs in Neuroinflammation: Implications in Disease Pathogenesis, Biomarker Discovery and Therapeutic Applications
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Lymph nodes are innervated by a unique population of sensory neurons with immunomodulatory potential
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PDGFRβ Cells Rapidly Relay Inflammatory Signal from the Circulatory System to Neurons via Chemokine CCL2
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Viral Encephalitis and Neurologic Diseases: Focus on Astrocytes
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Toxoplasmosis: A pathway to neuropsychiatric disorders
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Astrocyte-derived lipoxins A4 and B4 promote neuroprotection from acute and chronic injury
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Neurogranin: A Potential Biomarker of Neurological and Mental Diseases
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Δ9-Tetrahydrocannabinol Suppresses Monocyte-Mediated Astrocyte Production of Monocyte Chemoattractant Protein 1 and Interleukin-6 in a Toll-Like Receptor 7–Stimulated Human Coculture
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Neuroprotective Strategies in Aneurysmal Subarachnoid Hemorrhage (aSAH)
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Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection
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The Use of Antimicrobial and Antiviral Drugs in Alzheimer’s Disease
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Modulation of MicroRNAs as a Potential Molecular Mechanism Involved in the Beneficial Actions of Physical Exercise in Alzheimer Disease
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The Early Innate Immune Response to, and Phagocyte-Dependent Entry of, Cryptococcus neoformans Map to the Perivascular Space of Cortical Post-Capillary Venules in Neurocryptococcosis
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Drosophila as a Model to Study Brain Innate Immunity in Health and Disease
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Inflammasomes in CNS Diseases
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A congenital CMV infection model for follow-up studies of neurodevelopmental disorders, neuroimaging abnormalities, and treatment
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Intrauterine Viral Infections: Impact of Inflammation on Fetal Neurodevelopment
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CA-30, an oligosaccharide fraction derived from Liuwei Dihuang decoction, ameliorates cognitive deterioration via the intestinal microbiome in the senescence-accelerated mouse prone 8 strain
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Gut Microbiota Dynamics in Relation to Long-COVID-19 Syndrome: Role of Probiotics to Combat Psychiatric Complications
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Systemic Response to Infection Induces Long-Term Cognitive Decline: Neuroinflammation and Oxidative Stress as Therapeutical Targets
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Non-coding RNAs: The Neuroinflammatory Regulators in Neurodegenerative Diseases
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Authors: Klein, R. S., Garber, C., & Howard, N.
Affiliations: Washington University in St. Louis (US)
Corresponding author: Klein, Robyn S
ORCID: Klein, Robyn S
Garber, Charise
Howard, Nicole
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2017-01-16
Volume: 18
Issue: 2
Pages: 132-141
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.3656
PMC: PMC5815515
OpenAlex: W2576931861
Cited by: 235
References: 178
Citations by year: 2026: 13 · 2025: 24 · 2024: 23 · 2023: 25 · 2022: 22 · 2021: 49 · 2020: 37 · 2019: 15 · 2018: 15 · 2017: 12
FWCI: 2.08
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Multiple Sclerosis Society
National Institutes of Health
National Heart, Lung, and Blood Institute (T32HL007317)
National Institute of Allergy and Infectious Diseases (R01AI126909, U19AI083019, R21AI114549, R01AI101400)
National Institute of Neurological Disorders and Stroke (P01NS059560, UH2NS100126, R01NS052632)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Infectious Diseases › Infectious Encephalopathies and Encephalitis
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords: neuroinflammation, central nervous system infection, brain function, mental status, mental illness, neurodegenerative diseases
MeSH terms: Animals, Brain, Central Nervous System, Humans, Immunity, Nervous System Diseases, Virus Diseases, Neuroimmunomodulation, Viral Load, Neurogenic Inflammation

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Infectious immunity in the central nervous system and brain function

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