ArticleNaunyn-Schmiedeberg's archives of pharmacology2011
Difference in the biological effects of Clostridium difficile toxin B in proliferating and non-proliferating cells.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 24 citations in OpenAlex.
- The Essential Role of Rac1 Glucosylation inFrontiers in microbiology · 2022Article
- Inhibition of Clostridium difficile TcdA and TcdB toxins with transition state analogues.Nature communications · 2021Article
- Article
- Article
- Difference in Mono-O-Glucosylation of Ras Subtype GTPases Between Toxin A and Toxin B FromFrontiers in microbiology · 2018Article
- Transforming Growth Factor β1/SMAD Signaling Pathway Activation Protects the Intestinal Epithelium from Clostridium difficile Toxin A-Induced Damage.Infection and immunity · 2017Article
- Glucosyltransferase Activity of Clostridium difficile Toxin B Triggers Autophagy-mediated Cell Growth Arrest.Scientific reports · 2017Article
- Role of p38Toxins · 2016Article
- Clostridium difficile Toxins TcdA and TcdB Cause Colonic Tissue Damage by Distinct Mechanisms.Infection and immunity · 2016Article
- Pathogenic effects of glucosyltransferase from Clostridium difficile toxins.Pathogens and disease · 2016Review
- Reactive Oxygen Species as Additional Determinants for Cytotoxicity of Clostridium difficile Toxins A and B.Toxins · 2016Review
- DXD motif-dependent and -independent effects of the chlamydia trachomatis cytotoxin CT166.Toxins · 2015Article
- Clostridium difficile toxin A attenuates Wnt/β-catenin signaling in intestinal epithelial cells.Infection and immunity · 2014Article
- Probiotics for the treatment of Clostridium difficile associated disease.World journal of gastrointestinal pathophysiology · 2013Article
- Article
- The P2Y6 receptor mediates Clostridium difficile toxin-induced CXCL8/IL-8 production and intestinal epithelial barrier dysfunction.PloS one · 2013Article
- Clostridium difficile Toxin B causes epithelial cell necrosis through an autoprocessing-independent mechanism.PLoS pathogens · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toxin A (TcdA) and toxin B (TcdB) from Clostridium difficile are the causative agents of the C. difficile-associated diarrhea (CDAD) and its severe form, the pseudomembranous colitis. TcdA and TcdB both glucosylate and thereby inactivate low molecular weight GTP-binding proteins of the Rho, Rac, and Cdc42 subfamilies. In cultured cell lines, TcdB induces actin re-organization and bi-nucleation ("cytopathic effects") and cell death ("cytotoxic effects"). In this study, the role of cell cycle progression in the cytopathic and the cytotoxic effects of TcdB is evaluated by a differential analysis of these effects in proliferating and non-proliferating cells. Density-synchronized murine fibroblasts and confluent HT29 colonocytes are exploited as cell culture models for non-proliferating cells. Cell death is analyzed in terms of a loss of cell viability, phosphatidylserine exposure, and DNA fragmentation. In proliferating cells, TcdB blocks cell proliferation and induces apoptotic cell death. In contrast, TcdB induces non-apoptotic cell death in non-proliferating cells. TcdB-induced cell rounding turns out to be independent of cell cycle progression. Cell cycle progression is an important determinant in the biological effects of TcdB. With respect to the pathology of CDAD, this study leads to the new hypothesis that necrotic cell death of terminally differentiated colonocytes and inhibition of epithelial renewal of the colon contribute to the pathogenesis of CDAD.
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.