ArticleJournal of neuroinflammation2014
MiR-155 induction in microglial cells suppresses Japanese encephalitis virus replication and negatively modulates innate immune responses.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 120 citations in OpenAlex.
- Japanese Encephalitis Virus and Host Innate Immunity: Insights Into TLR Signaling, PRR Crosstalk, and Viral Immune Evasion.Cell biochemistry and function · 2026Review
- Neuroinflammation and blood-brain barrier disruption in Japanese encephalitis virus infection: mechanisms, therapeutic targets, and intervention strategies.Archives of pharmacal research · 2026Review
- Myeloid miR-155 deficiency exacerbates viral encephalitis by hindering M1 macrophage polarization due to impaired NLRP3 inflammasome activation in extraneural tissues.Frontiers in immunology · 2026Article
- Pathways in the brain, heart and lung influenced by SARS-CoV-2 NSP6 and SARS-CoV-2 regulated miRNAs: an in silico study hinting cancer incidence.Cardio-oncology (London, England) · 2025Article
- Interferon and immunity: the role of microRNA in viral evasion strategies.Frontiers in immunology · 2025Review
- Computational Screening to Predict MicroRNA Targets in the Flavivirus 3' UTR Genome: An Approach for Antiviral Development.International journal of molecular sciences · 2024Article
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- Toward a Categorization of Virus-ncRNA Interactions in the World of RNA to Disentangle the Tiny Secrets of Dengue Virus.Viruses · 2024Review
- TGFβ1-induced hedgehog signaling suppresses the immune response of brain microvascular endothelial cells elicited by meningitic Escherichia coli.Cell communication and signaling : CCS · 2024Article
- Review
- miR-155 facilitates the synergistic replication between avian leukosis virus subgroup J and reticuloendotheliosis virus by targeting a dual pathway.Journal of virology · 2023Article
- Emerging role of non-coding RNAs in neuroinflammation mediated by microglia and astrocytes.Journal of neuroinflammation · 2023Review
- Review
- Systemic Listeria monocytogenes infection in aged mice induces long-term neuroinflammation: the role of miR-155.Immunity & ageing : I & A · 2022Article
- MicroRNAs as Regulators of Phagocytosis.Cells · 2022Review
- The Complement System in the Central Nervous System: From Neurodevelopment to Neurodegeneration.Biomolecules · 2022Review
- Modes of action and diagnostic value of miRNAs in sepsis.Frontiers in immunology · 2022Review
- Regulatory Role of Host MicroRNAs in Flaviviruses Infection.Frontiers in microbiology · 2022Review
- miR-155: An Important Role in Inflammation Response.Journal of immunology research · 2022Review
- Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroglial cells, which are resident macrophages of the central nervous system, play important roles in immune responses and pathogenesis. Japanese encephalitis virus (JEV) is a neurotropic virus that infects microglial cells in brain. Several microRNAs including miR-155 and miR-146a play an important role in defining the microglia inflammatory profile. In this study, we have investigated the effect of miR-155 and miR-146a modulation on JEV infection as well as innate immune responses in human microglial cells.
methodsIn vitro studies were performed in JEV-infected human microglial CHME3 cells. miR-155 or miR-146a were overexpressed and total RNA and protein were extracted following JEV-infection. Expression of genes involved in innate immune responses was studied by PCR array, quantitative real-time PCR (qPCR), western blot and Fluorescence activated cell sorter (FACS). JEV replication was monitored by studying the viral RNA by qPCR, protein by western blot, and titres by plaque assay.
resultsOverexpression of miR-155 in CHME3 cells resulted in significantly reduced JEV replication whereas miR-146a overexpression had an insignificant effect. Additionally, interferon regulatory factor 8 (IRF8) and complement factor H (CFH) were induced during JEV infection; however, this induction was attenuated in miR-155 overexpressing cells following JEV infection. Further, JEV-induced NF-κB regulated downstream gene expression was attenuated. Interestingly, an increased level of CD45, a negative regulator of microglia activation and a reduced phosphorylated-Signal Transducers and Activators of Transcription (p-STAT1) expression was observed in miR-155 overexpressing cells upon JEV infection.
conclusionInduction of miR-155 in human microglial cells may negatively modulate JEV-induced innate immune gene expression and may have a beneficial role in limiting JEV replication in human microglial cells.
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