ArticleScientific reports2019
Human TNF-Luc reporter mouse: A new model to quantify inflammatory responses.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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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.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Macrophage-Specific NF-κB Activation Dynamics Can Segregate Inflammatory Bowel Disease Patients.Frontiers in immunology · 2019Trial
- Intercellular model predicts mechanisms of inflammation-fibrosis coupling after myocardial infarction.The Journal of physiology · 2023Article
- Selenium intracanal dressing: effects on the periapical immune response.Clinical oral investigations · 2021Article
- Impact of Interleukin 10 Deficiency on Intestinal Epithelium Responses to Inflammatory Signals.Frontiers in immunology · 2021Article
- Using systems medicine to identify a therapeutic agent with potential for repurposing in inflammatory bowel disease.Disease models & mechanisms · 2020Article
- The Generation of an Engineered Interleukin-10 Protein With Improved Stability and Biological Function.Frontiers in immunology · 2020Article
- Inhibition of CXCR4 and CXCR7 Is Protective in Acute Peritoneal Inflammation.Frontiers in immunology · 2020Article
- Replication of Crohn's Disease MucosalPathogens (Basel, Switzerland) · 2019Article
- Ubiquitous Luciferase Expression in "Firefly Rats" Does Not Alter the Pancreatic Islet Morphology, Metabolism, and Function.Cell transplantationArticle
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Tumour necrosis factor (TNF) is a key cytokine during inflammatory responses and its dysregulation is detrimental in many inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease. Here, we used a bacterial artificial chromosome (BAC) construct that expresses luciferase under the control of the human TNF locus to generate a novel transgenic mouse, the hTNF.LucBAC strain. In vitro stimulation of hTNF.LucBAC cells of different origin revealed a cell specific response to stimuli demonstrating the integrated construct's ability as a proxy for inflammatory gene response. Lipopolysaccharide was the most potent luciferase inducer in macrophages, while TNF was a strong activator in intestinal organoids. Lipopolysaccharide-induced luciferase activity in macrophages was downregulated by inhibitors of NF-κB pathway, as well as by Interleukin-10, a known anti-inflammatory cytokine. Moreover, the transgene-dependent luciferase activity showed a positive correlation to the endogenous murine soluble TNF secreted to the culture medium. In conclusion, the hTNF.LucBAC strain is a valuable tool for studying and screening molecules that target TNF synthesis and will allow further functional studies of the regulatory elements of the TNF locus.
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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.