ArticlePloS one2017
Treatment with the NR4A1 agonist cytosporone B controls influenza virus infection and improves pulmonary function in infected mice.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 28 citations in OpenAlex.
- Single-cell and spatial transcriptomic profiling reveals distinct immune landscapes in murine lungs infected with H1N1 versus H5N1 influenza viruses.Journal of virology · 2026Article
- Alleviation of experimental arthritis in SKG mice throughFrontiers in immunology · 2026Article
- Review
- Cytosporones Y and Z, new antifungal polyketides produced by the fungal strain Trichoderma sp. FKI-6626.The Journal of antibiotics · 2024Article
- Nur77 protects the bladder urothelium from intracellular bacterial infection.Nature communications · 2024Article
- Surface Chemistry of Cytosporone-B Incorporated in Models for Microbial Biomembranes as Langmuir Monolayers.Langmuir : the ACS journal of surfaces and colloids · 2024Article
- Biosynthesis of Cytosporones in Leotiomycetous Filamentous Fungi.Journal of the American Chemical Society · 2024Article
- SARS-CoV-2-infected human airway epithelial cell cultures uniquely lack interferon and immediate early gene responses caused by other coronaviruses.Clinical & translational immunology · 2024Article
- Identification of key genes as potential diagnostic and therapeutic targets for comorbidity of myasthenia gravis and COVID-19.Frontiers in neurology · 2023Article
- NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosis.Neural regeneration research · 2022Article
- Role of NR4A family members in myeloid cells and leukemia.Current research in immunology · 2022Article
- Article
- Nuclear Receptors in Asthma: Empowering Classical Molecules Against a Contemporary Ailment.Frontiers in immunology · 2020Review
- Cytosporone B as a Biological Preservative: Purification, Fungicidal Activity and Mechanism of Action againstBiomolecules · 2019Article
- Structurally Diverse Polyketides From the Mangrove-Derived FungusFrontiers in chemistry · 2018Article
- The Orphan Nuclear Receptor 4A1: A Potential New Therapeutic Target for Metabolic Diseases.Journal of diabetes research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor NR4A1 has emerged as a pivotal regulator of the inflammatory response and immune homeostasis. Although contribution of NR4A1 in the innate immune response has been demonstrated, its role in host defense against viral infection remains to be investigated. In the present study, we show that administration of cytosporone B (Csn-B), a specific agonist of NR4A1, to mice infected with influenza virus (IAV) reduces lung viral loads and improves pulmonary function. Our results demonstrate that administration of Csn-B to naive mice leads to a modest production of type 1 IFN. However, in IAV-infected mice, such production of IFNs is markedly increased following treatment with Csn-B. Our study also reveals that alveolar macrophages (AMs) appear to have a significant role in Csn-B effects, since selective depletion of AMs with clodronate liposome correlates with a marked reduction of IFN production, viral clearance and morbidity in IAV-infected mice. Furthermore, when reemergence of AMs is observed following clodronate liposome administration, an increased production of IFNs was detected in bronchoalveolar fluids of IAV-infected mice treated with Csn-B, supporting the contribution of AMs in Csn-B effects. While treatment of mice with Csn-B induces phosphorylation of transcriptional factors IRF3 and IRF7, the latter appears to be less indispensable since effects of Csn-B treatment on the synthesis of IFNs were slightly affected in IAV-infected mice lacking functional IRF7. Together, our results highlight the capacity of Csn-B and consequently of NR4A1 transcription factor in controlling IAV infection.
Indexed as
Identifiers
What Socratic 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 Socratic graph.