scholarly journals Innate Immune Sensing of Viruses and Its Consequences for the Central Nervous System

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 170
Author(s):  
Hina Singh ◽  
Jeffrey Koury ◽  
Marcus Kaul
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nerve Fibers ◽  
Innate Immune ◽  
Health Concern ◽  
Type I ◽  
Lectin Receptors ◽  
The Central Nervous System ◽  
Immune Sensing ◽  
Innate Immune Sensing

Viral infections remain a global public health concern and cause a severe societal and economic burden. At the organismal level, the innate immune system is essential for the detection of viruses and constitutes the first line of defense. Viral components are sensed by host pattern recognition receptors (PRRs). PRRs can be further classified based on their localization into Toll-like receptors (TLRs), C-type lectin receptors (CLR), retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), NOD-like receptors (NLRs) and cytosolic DNA sensors (CDS). TLR and RLR signaling results in production of type I interferons (IFNα and -β) and pro-inflammatory cytokines in a cell-specific manner, whereas NLR signaling leads to the production of interleukin-1 family proteins. On the other hand, CLRs are capable of sensing glycans present in viral pathogens, which can induce phagocytic, endocytic, antimicrobial, and pro- inflammatory responses. Peripheral immune sensing of viruses and the ensuing cytokine response can significantly affect the central nervous system (CNS). But viruses can also directly enter the CNS via a multitude of routes, such as the nasal epithelium, along nerve fibers connecting to the periphery and as cargo of infiltrating infected cells passing through the blood brain barrier, triggering innate immune sensing and cytokine responses directly in the CNS. Here, we review mechanisms of viral immune sensing and currently recognized consequences for the CNS of innate immune responses to viruses.

scholarly journals Exosomes Secreted by Microglia During Virus Infection in the Central Nervous System Activate an Inflammatory Response in Bystander Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Nhungoc Luong ◽  
Julie K. Olson
Keyword(s):  
Central Nervous System ◽  
Immune Response ◽  
Nervous System ◽  
Demyelinating Disease ◽  
Innate Immune ◽  
Viral Rna ◽  
Type I Interferons ◽  
Type I ◽  
The Central Nervous System ◽  
Bystander Cells

Microglia become persistently infected during Theiler’s murine encephalomyelitis virus (TMEV) infection in the central nervous system (CNS) of susceptible mice. We have previously shown that microglia infected with TMEV become activated through the innate immune receptors to express type I interferons, cytokines, and chemokines. Persistent TMEV infection in the CNS promotes chronic neuroinflammation and development of demyelinating disease similar to multiple sclerosis. In the current studies, we wanted to determine whether TMEV-infected microglia secrete exosomes which contribute to neuroinflammation in the CNS thus promoting the development of demyelinating disease. Exosomes are vesicles containing RNA, DNA, and proteins that are released from one cell and taken up by another cell to facilitate communication between cells. These studies isolated exosomes secreted by microglia during TMEV infection in vitro as well as exosomes secreted by microglia during early TMEV infection in mice. These studies show that microglia secrete exosomes during TMEV infection which contain the viral RNA coding region. The exosomes secreted by microglia during TMEV infection can be taken up by uninfected bystander cells, including CNS resident microglia, astrocytes, and neurons. The viral RNA in the exosomes can be transferred to the bystander cells. In addition, the bystander cells that took up these exosomes were activated through the innate immune response to express type I interferons, IFNα and IFNβ, pro-inflammatory cytokines, IL-6, IL-12, and TNFα, and chemokines, CCL2. Most interestingly, exosomes secreted by microglia during early TMEV infection in mice activated an inflammatory response when transferred to the brains of naïve mice. These results show that exosomes secreted by microglia during early TMEV infection contain viral RNA and can activate uninfected bystander CNS cells to promote an inflammatory immune response. Thus, exosomes secreted by microglia during virus infection may promote viral persistence and neuroinflammation which contributes to the development of demyelinating disease.

Innate Immune Surveillance in the Central Nervous System Following Legionella pneumophila Infection

2018 ◽  
Vol 16 (10) ◽  
pp. 1080-1089 ◽  
Author(s):  
Pasqualina Lagana ◽  
Luca Soraci ◽  
Maria Elsa Gambuzza ◽  
Giuseppe Mancuso ◽  
Santi Antonino Delia
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Legionella Pneumophila ◽  
Immune Surveillance ◽  
Innate Immune ◽  
The Central Nervous System

Understanding Neuropathic Pain

CNS Spectrums ◽  
2005 ◽  
Vol 10 (4) ◽  
pp. 298-308 ◽  
Author(s):  
Walter Zieglgänsberger ◽  
Achim Berthele ◽  
Thomas R. Tölle
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Neuronal Excitability ◽  
Traumatic Injury ◽  
Nerve Fibers ◽  
Cellular Events ◽  
Excitatory Neurotransmitters ◽  
The Central Nervous System ◽  
Activity Dependent

AbstractNeuropathic pain is defined as a chronic pain condition that occurs or persists after a primary lesion or dysfunction of the peripheral or central nervous system. Traumatic injury of peripheral nerves also increases the excitability of nociceptors in and around nerve trunks and involves components released from nerve terminals (neurogenic inflammation) and immunological and vascular components from cells resident within or recruited into the affected area. Action potentials generated in nociceptors and injured nerve fibers release excitatory neurotransmitters at their synaptic terminals such as L-glutamate and substance P and trigger cellular events in the central nervous system that extend over different time frames. Short-term alterations of neuronal excitability, reflected for example in rapid changes of neuronal discharge activity, are sensitive to conventional analgesics, and do not commonly involve alterations in activity-dependent gene expression. Novel compounds and new regimens for drug treatment to influence activity-dependent long-term changes in pain transducing and suppressive systems (pain matrix) are emerging.

scholarly journals Schwannoma of the arythenoid

2013 ◽  
Vol 11 (2) ◽  
pp. 224-226 ◽  
Author(s):  
Carlos Eduardo Molinari Nardi ◽  
Alexandre Wakil Burzichelli ◽  
Elio Gilberto Pfuetzenreiter ◽  
Rogerio Aparecido Dedivitis
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Rare Case ◽  
Nerve Fibers ◽  
Endoscopic Procedure ◽  
The Central Nervous System

Schwannoma is a benign encapsulated tumor that originates from the Schwann cells lining nerve fibers outside the central nervous system. We report a rare case of schwannoma that arose from the left arythenoid cartilage The patient underwent excision of the mass through microlaryngeal endoscopic procedure. No recurrence was observed during follow-up.

scholarly journals Differential Effects of Three CanonicalToxoplasmaStrains on Gene Expression in Human Neuroepithelial Cells

2010 ◽  
Vol 79 (3) ◽  
pp. 1363-1373 ◽  
Author(s):  
Jianchun Xiao ◽  
Lorraine Jones-Brando ◽  
C. Conover Talbot ◽  
Robert H. Yolken
Keyword(s):  
Gene Expression ◽  
Central Nervous System ◽  
Nervous System ◽  
Nucleotide Metabolism ◽  
Neural Cells ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Neuroepithelial Cells ◽  
The Central Nervous System

ABSTRACTStrain type is one of the key factors suspected to play a role in determining the outcome ofToxoplasmainfection. In this study, we examined the transcriptional profile of human neuroepithelioma cells in response to representative strains ofToxoplasmaby using microarray analysis to characterize the strain-specific host cell response. The study of neural cells is of interest in light of the ability ofToxoplasmato infect the brain and to establish persistent infection within the central nervous system. We found that the extents of the expression changes varied considerably among the three strains. Neuroepithelial cells infected withToxoplasmatype I exhibited the highest level of differential gene expression, whereas type II-infected cells had a substantially smaller number of genes which were differentially expressed. Cells infected with type III exhibited intermediate effects on gene expression. The three strains also differed in the individual genes and gene pathways which were altered following cellular infection. For example, gene ontology (GO) analysis indicated that type I infection largely affects genes related to the central nervous system, while type III infection largely alters genes which affect nucleotide metabolism; type II infection does not alter the expression of a clearly defined set of genes. Moreover, Ingenuity Pathways Analysis (IPA) suggests that the three lineages differ in the ability to manipulate their host; e.g., they employ different strategies to avoid, deflect, or subvert host defense mechanisms. These observed differences may explain some of the variation in the neurobiological effects of different strains ofToxoplasmaon infected individuals.

Immunology of Multiple Sclerosis

2016 ◽  
Author(s):  
Laura Piccio ◽  
Anne H. Cross
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Monoclonal Antibodies ◽  
B Lymphocytes ◽  
Autoimmune Disorder ◽  
Innate Immune ◽  
Immune Systems ◽  
The Central Nervous System ◽  
Multiple Sclerosis Treatment

Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system that targets myelin but affects both white matter and gray matter. Multiple sclerosis is thought to be mediated by cells of the adaptive and innate immune systems. CD4+ T lymphocytes of the Th1 and Th17 subtypes are believed to be critical for the initiation of multiple sclerosis. Treatment with monoclonal antibodies that deplete B lymphocytes has proven that B cells are critical to relapse development in multiple sclerosis. While immunopathophysiology is clearly important in MS, whether multiple sclerosis is truly an autoimmune disorder and the target or targets of the autoimmunity remain unknown.

scholarly journals TBK1, a central kinase in innate immune sensing of nucleic acids and beyond

2020 ◽  
Vol 52 (7) ◽  
pp. 757-767 ◽  
Author(s):  
Ruyuan Zhou ◽  
Qian Zhang ◽  
Pinglong Xu
Keyword(s):  
Nucleic Acids ◽  
Cell Biology ◽  
Innate Immune ◽  
Type I ◽  
Interferon Stimulated Genes ◽  
Immune Sensing ◽  
Mitochondrial Antiviral Signaling ◽  
I Kappa B Kinase ◽  
Innate Immune Sensing ◽  
Mitochondrial Antiviral Signaling Protein

Abstract Sensing of intracellular and extracellular environments is one of the fundamental processes of cell. Surveillance of aberrant nucleic acids, derived either from invading pathogens or damaged organelle, is conducted by pattern recognition receptors (PRRs) including RIG-I-like receptors, cyclic GMP-AMP synthase, absent in melanoma 2, and a few members of toll-like receptors. TANK-binding kinase 1 (TBK1), along with its close analogue I-kappa-B kinase epsilon, is a central kinase in innate adaptor complexes linking activation of PRRs to mobilization of transcriptional factors that transcribe proinflammatory cytokines, type I interferon (IFN-α/β), and myriads interferon stimulated genes. However, it still remains elusive for the precise mechanisms of activation and execution of TBK1 in signaling platforms formed by innate adaptors mitochondrial antiviral signaling protein (MAVS), stimulator of interferon genes protein (STING), and TIR-domain-containing adapter-inducing interferon-β (TRIF), as well as its complex regulations. An atlas of TBK1 substrates is in constant expanding, setting TBK1 as a key node of signaling network and a dominant player in contexts of cell biology, animal models, and human diseases. Here, we review recent advancements of activation, regulations, and functions of TBK1 under these physiological and pathological contexts.

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