ArticleInfection and immunity2016
Analysis of TcdB Proteins within the Hypervirulent Clade 2 Reveals an Impact of RhoA Glucosylation on Clostridium difficile Proinflammatory Activities.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
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- Characterizing host-microbe interactions with bacterial effector proteins using proximity-dependent biotin identification (BioID).Communications biology · 2025Review
- Allele-linked divergence in SlpA and TcdB drives distinct immune and cytotoxic responses that distinguish ST01 from non-ST01 strains in Clade 2 Clostridioides difficile.Access microbiology · 2025Article
- A sequence invariable region in TcdB2 is required for toxin escape fromJournal of bacteriology · 2024Article
- Genomic and phenotypic studies amongMicrobiology spectrum · 2024Article
- Exploring the Toxin-Mediated Mechanisms inMicroorganisms · 2024Review
- Comparative Genomics of Clostridioides difficile.Advances in experimental medicine and biology · 2024Article
- Article
- Host Immunity and Immunization Strategies for Clostridioides difficile Infection.Clinical microbiology reviews · 2023Review
- Clostridioides difficile toxins: mechanisms of action and antitoxin therapeutics.Nature reviews. Microbiology · 2022Review
- Structural basis for selective modification of Rho and Ras GTPases byScience advances · 2021Article
- Large Clostridial Toxins: Mechanisms and Roles in Disease.Microbiology and molecular biology reviews : MMBR · 2021Review
- Exoproteomic analysis of two MLST clade 2 strains of Clostridioides difficile from Latin America reveal close similarities.Scientific reports · 2021Article
- Functional analyses of epidemic Clostridioides difficile toxin B variants reveal their divergence in utilizing receptors and inducing pathology.PLoS pathogens · 2021Article
- Subtyping analysis reveals new variants and accelerated evolution of Clostridioides difficile toxin B.Communications biology · 2020Article
- In vivo animal models confirm an increased virulence potential and pathogenicity of the NAP1/RT027/ST01 genotype within theGut pathogens · 2020Article
- Epidemiology and virulence-associated genes ofAccess microbiology · 2020Article
- Toxin B Variants fromToxins · 2019Article
- Hypervirulent clade 2, ribotype 019/sequence type 67Gut pathogens · 2019Article
- The role of toxins in Clostridium difficile infection.FEMS microbiology reviews · 2017Review
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Clostridium difficile strains within the hypervirulent clade 2 are responsible for nosocomial outbreaks worldwide. The increased pathogenic potential of these strains has been attributed to several factors but is still poorly understood. During a C. difficile outbreak, a strain from this clade was found to induce a variant cytopathic effect (CPE), different from the canonical arborizing CPE. This strain (NAP1V) belongs to the NAP1 genotype but to a ribotype different from the epidemic NAP1/RT027 strain. NAP1V and NAP1 share some properties, including the overproduction of toxins, the binary toxin, and mutations in tcdC. NAP1V is not resistant to fluoroquinolones, however. A comparative analysis of TcdB proteins from NAP1/RT027 and NAP1V strains indicated that both target Rac, Cdc42, Rap, and R-Ras but only the former glucosylates RhoA. Thus, TcdB from hypervirulent clade 2 strains possesses an extended substrate profile, and RhoA is crucial for the type of CPE induced. Sequence comparison and structural modeling revealed that TcdBNAP1 and TcdBNAP1V share the receptor-binding and autoprocessing activities but vary in the glucosyltransferase domain, consistent with the different substrate profile. Whereas the two toxins displayed identical cytotoxic potencies, TcdBNAP1 induced a stronger proinflammatory response than TcdBNAP1V as determined in ex vivo experiments and animal models. Since immune activation at the level of intestinal mucosa is a hallmark of C. difficile-induced infections, we propose that the panel of substrates targeted by TcdB is a determining factor in the pathogenesis of this pathogen and in the differential virulence potential seen among C. difficile strains.
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