ArticlePLoS pathogens2013
Clostridium difficile 027/BI/NAP1 encodes a hypertoxic and antigenically variable form of TcdB.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 85 citations in OpenAlex.
- Substance P receptor blockade is associated with increased survival of patients withbioRxiv : the preprint server for biology · 2026Article
- The impact of TcdB conformational dynamics on vaccination against Clostridioides difficile.PLoS pathogens · 2026Article
- IL-33 protects from recurrent C. difficile infection by restoration of humoral immunity.The Journal of clinical investigation · 2025Article
- Mechanisms ofFrontiers in cellular and infection microbiology · 2025Review
- Prevalence of toxigenicThe Libyan journal of medicine · 2024Article
- Whole-Genome Sequencing-Based Characterization ofMicroorganisms · 2024Article
- IL-33 protects from recurrentbioRxiv : the preprint server for biology · 2024Article
- Bacterial toxins induce non-canonical migracytosis to aggravate acute inflammation.Cell discovery · 2024Article
- A sequence invariable region in TcdB2 is required for toxin escape fromJournal of bacteriology · 2024Article
- Review
- Exploring the Toxin-Mediated Mechanisms inMicroorganisms · 2024Review
- CSPG4-dependent cytotoxicity formSphere · 2024Article
- Testing and Diagnosis of Clostridioides difficile Infection in Special Scenarios: A Systematic Review.Cureus · 2024Review
- Comparative genome analyses of clinical and non-clinicalFrontiers in microbiology · 2024Article
- Article
- Clostridioides (Clostridium) difficile: A silent nosocomial pathogen.Saudi medical journal · 2023Review
- Receptor binding mechanisms of Clostridioides difficile toxin B and implications for therapeutics development.The FEBS journal · 2023Review
- Low-toxinEmerging microbes & infections · 2022Article
- Identification of TFPI as a receptor reveals recombination-driven receptor switching in Clostridioides difficile toxin B variants.Nature communications · 2022Article
- Detection of Newly Secreted Antibodies Predicts Nonrecurrence in Primary Clostridioides difficile Infection.Journal of clinical microbiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The Clostridium difficile exotoxin, TcdB, which is a major virulence factor, varies between strains of this pathogen. Herein, we show that TcdB from the epidemic BI/NAP1/027 strain of C. difficile is more lethal, causes more extensive brain hemorrhage, and is antigenically variable from TcdB produced by previously studied strains of this pathogen (TcdB003). In mouse intoxication assays, TcdB from a ribotype 027 strain (TcdB027) was at least four fold more lethal than TcdB003. TcdB027 caused a previously undescribed brain hemorrhage in mice and this correlated with a heightened sensitivity of brain microvascular endothelial cells to the toxin. TcdB003 and TcdB027 also differed in their antigenic profiles and did not share cross-neutralizing epitopes in a major immunogenic region of the protein. Solid phase humoral mapping of epitopes in the carboxy-terminal domains (CTD) of TcdB027 and TcdB003 identified 11 reactive epitopes that varied between the two forms of TcdB, and 13 epitopes that were shared or overlapping. Despite the epitope differences and absence of neutralizing epitopes in the CTD of TcdB027, a toxoid form of this toxin primed a strong protective response. These findings indicate TcdB027 is a more potent toxin than TcdB003 as measured by lethality assays and pathology, moreover the sequence differences between the two forms of TcdB alter antigenic epitopes and reduce cross-neutralization by antibodies targeting the CTD.
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.