ArticleMediators of inflammation2015
Dengue Virus Infection Causes the Activation of Distinct NF-κB Pathways for Inducible Nitric Oxide Synthase and TNF-α Expression in RAW264.7 Cells.
Article in Mediators of inflammation, 2015. 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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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Monocyte TLR2/4 as predictive biomarkers for progression from dengue warning signs to severe disease.Frontiers in immunology · 2026Article
- In-silico discovery of druggable molecular signatures that drive dengue fever to severe dengue fever highlighting common pathogenesis through single-cell RNA-Seq analysis.Scientific reports · 2025Article
- Genetic Association Studies ofDiagnostics (Basel, Switzerland) · 2023Article
- Structural Characterization and Immunobiological Activity of Polysaccharides from Astragalus Oyster Mushroom.Molecules (Basel, Switzerland) · 2023Article
- Article
- Negative regulation of type I interferon signaling by integrin-linked kinase permits dengue virus replication.PLoS pathogens · 2023Article
- Cepharanthine inhibits dengue virus production and cytokine secretion.Virus research · 2023Article
- Review
- Multi-Tissue Transcriptomic-Informed In Silico Investigation of Drugs for the Treatment of Dengue Fever Disease.Viruses · 2021Article
- Role of endothelial cell receptors in the context of SARS-CoV-2 infection (COVID-19).Proceedings (Baylor University. Medical Center) · 2021Article
- Contact System Activation in Plasma from Dengue Patients Might Harness Endothelial Virus Replication through the Signaling of Bradykinin Receptors.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Antiviral Role of Phenolic Compounds against Dengue Virus: A Review.Biomolecules · 2020Review
- Specific Biomarkers Associated With Neurological Complications and Congenital Central Nervous System Abnormalities From Zika Virus-Infected Patients in Brazil.The Journal of infectious diseases · 2017Article
- Activation of Nrf2 by the dengue virus causes an increase in CLEC5A, which enhances TNF-α production by mononuclear phagocytes.Scientific reports · 2016Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with dengue virus (DENV) causes an increase in proinflammatory responses, such as nitric oxide (NO) generation and TNF-α expression; however, the molecular mechanism underlying this inflammatory activation remains undefined, although the activation of the transcription factor NF-κB is generally involved. In addition to TNF-α production in DENV-infected murine macrophage RAW264.7 cells, inducible NO synthase was transcriptionally and posttranslationally elevated and accompanied by NO generation. NF-κB is known to be activated by DENV infection. Pharmacologically inhibiting NF-κB activation abolishes iNOS/NO biosynthesis and TNF-α production. With inhibition, the potential role of NF-κB in oxidative signaling regulation was prevented during DENV infection. Heat-inactivated DENV failed to cause the identified inflammatory responses. Pharmacological inhibition of TLR3 partly decreased NF-κB activation; however, it effectively abolished inducible iNOS/NO biosynthesis but did not inhibit TNF-α production. In contrast to TLR3, viral protein NS2B3 also independently contributed to NF-κB activation to regulate TNF-α production. These results show the distinct pathways for NF-κB activation caused by DENV infection individually for the regulation of iNOS/NO and TNF-α expression.
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