ArticleFrontiers in cellular neuroscience2020
CCR2 Inhibition Reduces Neurotoxic Microglia Activation Phenotype After Japanese Encephalitis Viral Infection.
Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 24 citations in OpenAlex.
- Antiviral and neuroprotective activity of diallyl disulfide in Japanese encephalitis virus-challenged SH-SY5Y cells: a post-treatment approach for greater specificity.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Opportunities and Challenges of mRNA and VLP Technologies for Pan-Flavivirus Vaccine Development: Focus on Conserved Quaternary Epitope Conformations.International journal of molecular sciences · 2026Review
- Viral Infection and the Blood-Brain Barrier: Molecular Research Insights and Therapies.The Journal of infectious diseases · 2025Review
- An immunocompetent mouse model revealed that congenital Zika virus infection disrupted hippocampal function by activating autophagy.Emerging microbes & infections · 2025Article
- The slow progression of Japanese encephalitis in aged mice is likely associated to B cell recruitment in the brain.Virologica Sinica · 2025Article
- A central role for CCR2 in monocyte recruitment and blood-brain barrier disruption during Usutu virus encephalitis.Journal of neuroinflammation · 2025Article
- Role of inflammatory cytokine burst in neuro-invasion of Japanese Encephalitis virus infection: an immunotherapeutic approaches.Journal of neurovirology · 2024Review
- Mice as an Animal Model for Japanese Encephalitis Virus Research: Mouse Susceptibility, Infection Route, and Viral Pathogenesis.Pathogens (Basel, Switzerland) · 2023Review
- Japanese Encephalitis Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Psychological stress induces depressive-like behavior associated with bone marrow-derived monocyte infiltration into the hippocampus independent of blood-brain barrier disruption.Journal of neuroinflammation · 2022Article
- Pathogenicity and virulence of Japanese encephalitis virus: Neuroinflammation and neuronal cell damage.Virulence · 2021Review
- Article
- Neutrophil Recruitment and Participation in Severe Diseases Caused by Flavivirus Infection.Life (Basel, Switzerland) · 2021Review
- The Causes and Long-Term Consequences of Viral Encephalitis.Frontiers in cellular neuroscience · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Controlling the proinflammatory response of microglia by targeting chemokines (C-C motif) receptor 2 (CCR2) could be an important therapeutic approach for Japanese encephalitis virus (JEV) infection. Here, through JEV infection to BV2 microglia and young BALB/c mice, we investigated that CCR2 is highly upregulated after JEV infection and plays a key role in determining microglia activation phenotype and associated with neurotoxic proinflammatory mediators of TNF-α and IFNγ. In addition, we found JEV infection to BV2 microglia causes an increase in microglial proliferation and cell body area at day 1 and day 3. Using the agonist molecule of CCR2 inhibition; RS102895, significantly reduces microglia reactive phenotype and nitric oxide production. Further, to define the role of CCR2 in functional responses of microglia and their activation phenotype, we performed
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