ArticleInfection and immunity2016
Glucosylation Drives the Innate Inflammatory Response to Clostridium difficile Toxin A.
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 16 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
16 citing papers in PubMed, 28 citations in OpenAlex.
- A programmed reset mechanism primesScience advances · 2026Article
- Cysteine proteases and how YabG fits into clan CD of the MEROPS database.Journal of bacteriology · 2025Review
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- Exploring the Toxin-Mediated Mechanisms inMicroorganisms · 2024Review
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- Peroxisome proliferator-activated receptor-γ as the gatekeeper of tight junction inFrontiers in microbiology · 2022Article
- Large Clostridial Toxins: Mechanisms and Roles in Disease.Microbiology and molecular biology reviews : MMBR · 2021Review
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- The pyrin inflammasome in host-microbe interactions.Current opinion in microbiology · 2020Review
- Enterotoxic Clostridia:Microbiology spectrum · 2019Review
- Protective Effect ofFrontiers in microbiology · 2018Article
- How to rewire the host cell: A home improvement guide for intracellular bacteria.The Journal of cell biology · 2017Review
- The role of toxins in Clostridium difficile infection.FEMS microbiology reviews · 2017Review
- Cytokines Are Markers of the Clostridium difficile-Induced Inflammatory Response and Predict Disease Severity.Clinical and vaccine immunology : CVI · 2017Article
- Pathobionts: mechanisms of survival, expansion, and interaction with host with a focus onGut microbesArticle
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 2 institutions in 1 country.
Funding
Abstract
Clostridium difficile is a major, life-threatening hospital-acquired pathogen that causes mild to severe colitis in infected individuals. The tissue destruction and inflammation which characterize C. difficile infection (CDI) are primarily due to the Rho-glucosylating toxins A and B. These toxins cause epithelial cell death and induce robust inflammatory signaling by activating the transcription factor NF-κB, leading to chemokine and cytokine secretion. The toxins also activate the inflammasome complex, which leads to secretion of the pyrogenic cytokine IL-1β. In this study, we utilized glucosylation-deficient toxin A to show that activation of the inflammasome by this toxin is dependent on Rho glucosylation, confirming similar findings reported for toxin B. We also demonstrated that tissue destruction and in vivo inflammatory cytokine production are critically dependent on the enzymatic activity of toxin A, suggesting that inhibiting toxin glucosyltransferase activity may be effective in combating this refractory disease.
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.