The Innate Immune Response in the Central Nervous System and Its Role in Glioma Immune Surveillance

2004 ◽  
Vol 27 (5) ◽  
pp. 487-491 ◽  
Author(s):  
M.A. Friese ◽  
A. Steinle ◽  
M. Weller
Keyword(s):  
Central Nervous System ◽  
Immune Response ◽  
Nervous System ◽  
Innate Immune Response ◽  
Immune Surveillance ◽  
Innate Immune ◽  
The Central Nervous System

scholarly journals Complement C1q and C3 Are Critical for the Innate Immune Response toStreptococcus pneumoniaein the Central Nervous System

2007 ◽  
Vol 178 (3) ◽  
pp. 1861-1869 ◽  
Author(s):  
Tobias A. Rupprecht ◽  
Barbara Angele ◽  
Matthias Klein ◽  
Juergen Heesemann ◽  
Hans-Walter Pfister ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Immune Response ◽  
Nervous System ◽  
Innate Immune Response ◽  
Innate Immune ◽  
The Central Nervous System ◽  
Complement C1q

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

scholarly journals Polyamines play a critical role in the control of the innate immune response in the mouse central nervous system

2003 ◽  
Vol 162 (2) ◽  
pp. 257-268 ◽  
Author(s):  
Denis Soulet ◽  
Serge Rivest
Keyword(s):  
Central Nervous System ◽  
Immune Response ◽  
Nervous System ◽  
Innate Immune Response ◽  
Transcriptional Activation ◽  
Critical Role ◽  
Innate Immune ◽  
Genes Encoding ◽  
Factor Α ◽  
Mouse Central Nervous System

The present work investigated whether polyamines play a role in the control of the innate immune response in the brain. The first evidence that these molecules may be involved in such a process was based on the robust increase in the expression of the first and rate-limiting enzyme of biosynthesis of polyamines during immune stimuli. Indeed, systemic lipopolysaccharide (LPS) administration increased ornithine decarboxylase (ODC) mRNA and protein within neurons and microglia across the mouse central nervous system (CNS). This treatment was also associated with a robust and transient transcriptional activation of genes encoding pro-inflammatory cytokines and toll-like receptor 2 (TLR2) in microglial cells. The endotoxin increased the cerebral activity of ODC, which was abolished by a suicide inhibitor of ODC. The decrease in putrescine levels largely prevented the ability of LPS to trigger tumor necrosis factor α and TLR2 gene transcription in the mouse brain. In contrast, expression of both transcripts was clearly exacerbated in response to intracerebral spermine infusion. Finally, inhibition of polyamine synthesis abolished neurodegeneration and increased the survival rate of mice exposed to a model of severe innate immune reaction in the CNS. Thus, polyamines have a major impact on the neuronal integrity and cerebral homeostasis during immune insults.

scholarly journals The Crustacean Central Nervous System in Focus: Subacute Neurodegeneration Induces a Specific Innate Immune Response

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e80896 ◽  
Author(s):  
Paula Grazielle Chaves da Silva ◽  
Clynton Lourenço Corrêa ◽  
Sergio Luiz de Carvalho ◽  
Silvana Allodi
Keyword(s):  
Central Nervous System ◽  
Immune Response ◽  
Nervous System ◽  
Innate Immune Response ◽  
Innate Immune

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.

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