ArticleProceedings of the National Academy of Sciences of the United States of America2006
Identification of Clostridium difficile toxin B cardiotoxicity using a zebrafish embryo model of intoxication.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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.
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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Nonmammalian models to study Clostridioides difficile infection; a systematic review.Anaerobe · 2023Pooled it
- Trends and Impact ofGastroenterology research · 2026Article
- Review
- Review
- Clostridioides difficile toxin B subverts germinal center and antibody recall responses by stimulating a drug-treatable CXCR4-dependent mechanism.Cell reports · 2024Article
- Exploring the Toxin-Mediated Mechanisms inMicroorganisms · 2024Review
- Bacterial toxins and heart function: heat-labileBiophysical reviews · 2023Article
- p21-activated kinase 1 (PAK1) as a therapeutic target for cardiotoxicity.Archives of toxicology · 2022Review
- Human α-Defensin-6 NeutralizesInternational journal of molecular sciences · 2022Article
- Use of aFrontiers in immunology · 2021Article
- Extra-Intestinal Effects ofCells · 2020Article
- Bezlotoxumab for Preventing Recurrent Clostridioides difficile Infection: A Narrative Review from Pathophysiology to Clinical Studies.Infectious diseases and therapy · 2020Review
- Immunogenicity and Protection from Receptor-Binding Domains of Toxins as Potential Vaccine Candidates forVaccines · 2019Article
- The role of toxins in Clostridium difficile infection.FEMS microbiology reviews · 2017Review
- Article
- Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal Effects.Toxins · 2016Review
- 'Get in Early'; Biofilm and Wax Moth (Galleria mellonella) Models Reveal New Insights into the Therapeutic Potential of Clostridium difficile Bacteriophages.Frontiers in microbiology · 2016Article
- Article
- Chondroitin sulfate proteoglycan 4 functions as the cellular receptor for Clostridium difficile toxin B.Cell research · 2015Article
- Toxin-mediated paracellular transport of antitoxin antibodies facilitates protection against Clostridium difficile infection.Infection and immunity · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Clostridium difficile toxin B (TcdB) has been studied extensively by using cell-free systems and tissue culture, but, like many bacterial toxins, the in vivo targets of TcdB are unknown and have been difficult to elucidate with traditional animal models. In the current study, the transparent Danio rerio (zebrafish) embryo was used as a model for imaging of in vivo TcdB localization and organ-specific damage in real time. At 24 h after treatment, TcdB was found to localize at the pericardial region, and zebrafish exhibited the first signs of cardiovascular damage, including a 90% reduction in systemic blood flow and a 20% reduction in heart rate. Within 72 h of exposure to TcdB, the ventricle chamber of the heart became deformed and was unable to contract or pump blood, and the fish exhibited extensive pericardial edema. In line with the observed defects in ventricle contraction, TcdB was found to directly disrupt coordinated contractility and rhythmicity in primary cardiomyocytes. Furthermore, using a caspase-3 inhibitor, we were able to block TcdB-related cardiovascular damage and prevent zebrafish death. These findings present an insight into the in vivo targets of TcdB, as well as demonstrate the strength of the zebrafish embryo as a tractable model for identification of in vivo targets of bacterial toxins and evaluation of novel candidate therapeutics.
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Registered trials
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