ArticleNature microbiology2016
The binary toxin CDT enhances Clostridium difficile virulence by suppressing protective colonic eosinophilia.
Article in Nature microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
122 citing papers in PubMed, 1 synthesis or guideline pooled it, 185 citations in OpenAlex.
- Low eosinophils and their dynamic as a predictor of death in patients with infections: a systematic review and meta-analysis of cohort studies.Annals of medicine · 2025Pooled it
- From colonization to infection: Genomic evolution of Clostridioides difficile pathogenesis.Cell reports · 2026Review
- Review
- Balancing act of cytokines in controlling the severity ofInfection and immunity · 2026Review
- Biomarkers for Early Severity Prediction inMedicina (Kaunas, Lithuania) · 2026Review
- Antibiotics promote susceptibility tobioRxiv : the preprint server for biology · 2026Article
- Clostridioides difficile pathogenesis and control.Nature reviews. Microbiology · 2026Review
- Observational
- Clostridioides difficile : A suspected pro-carcinogenic bacterium for gastrointestinal tumors.Chinese medical journal · 2026Review
- Gut microbiota dysbiosis: Pathogenic drivers and emerging phage-based therapeutics.AIMS microbiology · 2026Review
- Exploring the etiology of colitis: insights from gut microbiota research.Gut microbes · 2025Review
- Article
- The Bordetella type III secretion system effector BteA targets host eosinophil-epithelial signaling to promote IL-1Ra expression and persistence.Communications biology · 2025Article
- The emerging view on the roles of butyrate inInfection and immunity · 2025Review
- Polysaccharide lyase PL3.3 possibly potentiating Clostridioides difficile clinical symptoms based on complete genome analysis of RT046/ST35 and RT012/ST54.International microbiology : the official journal of the Spanish Society for Microbiology · 2025Article
- Article
- The interplay between host immunity andmBio · 2025Review
- Oligomerization of the Clostridioides difficile transferase B component proceeds through a stepwise mechanism.PLoS pathogens · 2025Article
- Standard mouse diets lead to differences in severity in infectious and non-infectious colitis.mBio · 2025Article
- Review
62 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 4 countries.
Funding
Abstract
Clostridium difficile is the most common hospital acquired pathogen in the USA, and infection is, in many cases, fatal. Toxins A and B are its major virulence factors, but expression of a third toxin, known as C. difficile transferase (CDT), is increasingly common. An adenosine diphosphate (ADP)-ribosyltransferase that causes actin cytoskeletal disruption, CDT is typically produced by the major, hypervirulent strains and has been associated with more severe disease. Here, we show that CDT enhances the virulence of two PCR-ribotype 027 strains in mice. The toxin induces pathogenic host inflammation via a Toll-like receptor 2 (TLR2)-dependent pathway, resulting in the suppression of a protective host eosinophilic response. Finally, we show that restoration of TLR2-deficient eosinophils is sufficient for protection from a strain producing CDT. These findings offer an explanation for the enhanced virulence of CDT-expressing C. difficile and demonstrate a mechanism by which this binary toxin subverts the host immune response.
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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.