ArticleJournal of virology2004
Rabies virus stimulates nitric oxide production and CXC chemokine ligand 10 expression in macrophages through activation of extracellular signal-regulated kinases 1 and 2.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 63 citations in OpenAlex.
- Rabies virus uniquely reprograms the transcriptome of human monocyte-derived macrophages.Frontiers in cellular and infection microbiology · 2023Article
- Innate Immune Signaling and Role of Glial Cells in Herpes Simplex Virus- and Rabies Virus-Induced Encephalitis.Viruses · 2021Review
- Street RABV Induces the Cholinergic Anti-inflammatory Pathway in Human Monocyte-Derived Macrophages by Binding to nAChr α7.Frontiers in immunology · 2021Article
- Article
- Inhibition of MALT1 Decreases Neuroinflammation and Pathogenicity of Virulent Rabies Virus in Mice.Journal of virology · 2018Article
- Impact of caspase-1/11, -3, -7, or IL-1Cell death discovery · 2017Article
- Role of nitric oxide in the regulation of immune responses during rabies virus infection in mice.Virusdisease · 2016Article
- Subversion of the Immune Response by Rabies Virus.Viruses · 2016Review
- Profile of Cytokines and Chemokines Triggered by Wild-Type Strains of Rabies Virus in Mice.The American journal of tropical medicine and hygiene · 2016Article
- Correlation of inducible nitric oxide synthase (iNOS) inhibition with TNF-α, caspase-1, FasL and TLR-3 in pathogenesis of rabies in mouse model.Virus genes · 2016Article
- Systems Biomedicine of Rabies Delineates the Affected Signaling Pathways.Frontiers in microbiology · 2016Article
- Lymph node but not intradermal injection site macrophages are critical for germinal center formation and antibody responses to rabies vaccination.Journal of virology · 2015Article
- Antiviral potential of ERK/MAPK and PI3K/AKT/mTOR signaling modulation for Middle East respiratory syndrome coronavirus infection as identified by temporal kinome analysis.Antimicrobial agents and chemotherapy · 2015Article
- Expression of neuronal CXCL10 induced by rabies virus infection initiates infiltration of inflammatory cells, production of chemokines and cytokines, and enhancement of blood-brain barrier permeability.Journal of virology · 2015Article
- Human Bone Marrow-Derived Mesenchymal Stromal Cells Differentially Inhibit Cytokine Production by Peripheral Blood Monocytes Subpopulations and Myeloid Dendritic Cells.Stem cells international · 2015Article
- FC-98 regulates TLR9-mediated of CXCL-10 expression in dendritic cells via MAPK and STAT1 signaling pathway.BioMed research international · 2014Article
- Rabies virus glycoprotein is an important determinant for the induction of innate immune responses and the pathogenic mechanisms.Veterinary microbiology · 2013Article
- Passive carriage of rabies virus by dendritic cells.SpringerPlus · 2013Article
- The emerging role of CXCL10 in cancer (Review).Oncology letters · 2011Article
- CXCL10/IP-10 in infectious diseases pathogenesis and potential therapeutic implications.Cytokine & growth factor reviews · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages represent an essential part of innate immunity, and the viral infection of macrophages results in the release of multiple proinflammatory mediators, such as nitric oxide (NO), cytokines, and chemokines. This study was undertaken to define the molecular mechanism of macrophage activation in response to rabies virus (RV) infection. In RAW264 murine macrophage cells, a well-characterized macrophage model, RV replication was strictly restricted, whereas cell proliferation was significantly enhanced upon RV inoculation. Transcriptional analyses for the expression of inducible forms of NO synthase (iNOS), cytokines, and chemokines revealed that RV virions potentiate the gene expression of iNOS and CXC chemokine ligand 10 (CXCL10), a major chemoattractant of T helper cell type 1. However, RV stimulation had little or no effect on the expression profiles of proinflammatory cytokines and other types of chemokines. In macrophages stimulated with UV-inactivated RV virions, as well as infectious viruses, the phosphorylation of extracellular signal-regulated kinase (ERK) 1 and 2, members of the mitogen-activated protein kinase family, was significantly induced. Specific inhibitors of MAPK/ERK kinase reduced the RV-induced production of NO and CXCL10. Furthermore, the RV-induced activation of the ERK1/2 pathway was severely impaired by the neutralization of the endosomal and lysosomal pH environment with lysosomotropic agents, indicating that endocytosis is a key step leading to the activation of ERK1/2 signaling. Taken together, these results suggest that the ERK1/2-mediated signaling pathway plays a cardinal role in the selective activation of macrophages in response to RV virions, thereby regulating cellular functions during virus infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.