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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Nucleotide-binding oligomerization domain 1 (NOD1) regulates microglial activation in pseudorabies virus infection
Xiuxiu Sun1, Xinxin Jin1, Zhengdan Lin1
1Division of Veterinary Pathology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China.
Abstract:
The primary cause of viral encephalitis (VE) is invasion of the central nervous system (CNS) by the virus, which leads to neuroinflammation and poses a significant threat to global public health. Microglia, as CNS-resident macrophages, play a crucial role in neuroinflammation and are often identified as the preferred target for the prevention or treatment of VE. In this study, we used pseudorabies virus (PRV)-induced VE in mice and pigs as a model to investigate the regulation of microglial responses during viral encephalitis and explored the mechanism of microglial activation. Cellular experiments revealed that microglial activation was accompanied by cell migration, characteristic morphological changes, phagocytosis, inflammatory cytokine production, and antigen presentation. Transcriptome analysis revealed that genes related to inflammation in PRV-infected BV2 cells were significantly enriched. The expression of the NOD1 gene in BV2 cells was significantly increased during PRV infection, after which NOD1 in BV2 cells was silenced by siRNA and overexpressed via a plasmid. NOD1 was found to be involved in the secretion of cytokines in BV2 cells by regulating the MAPK/NF-κB signalling pathway. Mouse and pig experiments have shown that NOD1 is involved in the secretion of cytokines by microglia by regulating the MAPK/NF-κB signalling pathway during PRV infection.
Insights
This study reveals that NOD1 regulates microglial responses during viral encephalitis (VE) by controlling inflammatory cytokine secretion via the MAPK/NF-κB pathway. Understanding this mechanism offers new avenues for VE treatment targeting microglia.
Area of Science:
- Neuroscience
- Immunology
- Virology
Background:
- Viral encephalitis (VE) is a significant global health threat caused by viral invasion of the central nervous system (CNS).
- Microglia, the resident immune cells of the CNS, are critical players in neuroinflammation during VE and represent a key therapeutic target.
- Pseudorabies virus (PRV)-induced VE in animal models provides a platform to study microglial activation mechanisms.
Purpose of the Study:
- To investigate the regulatory mechanisms of microglial activation during viral encephalitis.
- To elucidate the role of NOD1 in microglial responses to PRV infection.
- To explore the signaling pathways involved in NOD1-mediated microglial activation.
Main Methods:
- Utilized a mouse and pig model of PRV-induced viral encephalitis.
- Performed cellular experiments on BV2 microglial cells, including gene silencing (siRNA) and overexpression (plasmid).
- Conducted transcriptome analysis to identify differentially expressed genes in PRV-infected cells.
- Investigated the involvement of the MAPK/NF-κB signaling pathway.
Main Results:
- Microglial activation during VE involved migration, morphological changes, phagocytosis, cytokine production, and antigen presentation.
- Transcriptome analysis of PRV-infected BV2 cells showed enrichment of inflammation-related genes.
- NOD1 expression was significantly upregulated in BV2 cells upon PRV infection.
- NOD1 modulated cytokine secretion in BV2 cells and microglia through the MAPK/NF-κB signaling pathway.
Conclusions:
- NOD1 plays a critical role in regulating microglial inflammatory responses during viral encephalitis.
- The MAPK/NF-κB signaling pathway is a key mediator of NOD1's function in microglia during PRV infection.
- Targeting NOD1 may offer a novel therapeutic strategy for managing viral encephalitis.
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