ArticleNature communications2018
Apoptosis of intestinal epithelial cells restricts Clostridium difficile infection in a model of pseudomembranous colitis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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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.
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Who cites it
55 citing papers in PubMed, 77 citations in OpenAlex.
- Proteolytic activation of executioner caspase-3 and -7 regulates different physiological processes in mice.The EMBO journal · 2026Article
- Host-Pathogen Interaction as a Driver of Cellular Senescence: Microbial Triggers and Host Response.International journal of molecular sciences · 2026Review
- Integrating machine learning and WGCNA to identify core candidate genes and decipher immune-related molecular networks in TcdA/TcdB-associated CDI.Antonie van Leeuwenhoek · 2026Article
- Evolutionary Genomics of Human Gut Bacteria: Ecological Plasticity Across the Mutualism-Pathogenicity Spectrum.International journal of molecular sciences · 2026Review
- Human non-canonical inflammasomes activate CASP3 to limit intracellular Salmonella replication in macrophages.PLoS pathogens · 2026Article
- Caspase-3/7 deficiency results in enhanced intestinal inflammation and reduced tumorigenesis.Science advances · 2026Article
- Modeling Clostridioides difficile toxin pathogenesis and antiserum protection in an immunocompetent intestine-on-chip platform.Scientific reports · 2026Article
- Immune Aspects of Clostridioides difficile Infection and Vaccine Development.Infectious disease clinics of North America · 2025Review
- Cross-kingdom dialogs in the gut: Integrating bacterial pathogens, helminths, and microbiota interactions for immune homeostasis.PLoS pathogens · 2025Review
- The interplay between host immunity andmBio · 2025Review
- Inhibitory effects of Levilactobacillus brevis IBRC-M10790 on apoptosis and inflammation induced by Clostridioides difficile culture supernatant in vitro.Scientific reports · 2025Article
- Modeling cancer-microbiome interactions in vitro: A guide to co-culture platforms.International journal of cancer · 2025Review
- Executioner caspases degrade essential mediators of pathogen-host interactions to inhibit growth of intracellular Listeria monocytogenes.Cell death & disease · 2025Article
- Mechanisms ofFrontiers in cellular and infection microbiology · 2025Review
- Bacterial toxins induce non-canonical migracytosis to aggravate acute inflammation.Cell discovery · 2024Article
- Loratadine as an Anti-inflammatory Agent Against Clostridium difficile Toxin B.The Journal of infectious diseases · 2024Article
- Review
- Exploring the Toxin-Mediated Mechanisms inMicroorganisms · 2024Review
- Prosurvival Pathway Protects From Clostridioides difficile Toxin-Mediated Cell Death.The Journal of infectious diseases · 2024Article
- Advancements in understanding bacterial enteritis pathogenesis through organoids.Molecular biology reports · 2024Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium difficile is the leading cause of pseudomembranous colitis in hospitalized patients. C. difficile enterotoxins TcdA and TcdB promote this inflammatory condition via a cytotoxic response on intestinal epithelial cells (IECs), but the underlying mechanisms are incompletely understood. Additionally, TcdA and TcdB engage the Pyrin inflammasome in macrophages, but whether Pyrin modulates CDI pathophysiology is unknown. Here we show that the Pyrin inflammasome is not functional in IECs and that Pyrin signaling is dispensable for CDI-associated IEC death and for in vivo pathogenesis. Instead, our studies establish that C. difficile enterotoxins induce activation of executioner caspases 3/7 via the intrinsic apoptosis pathway, and demonstrate that caspase-3/7-mediated IEC apoptosis is critical for in vivo host defense during early stages of CDI. In conclusion, our findings dismiss a critical role for inflammasomes in CDI pathogenesis, and identify IEC apoptosis as a host defense mechanism that restricts C. difficile infection in vivo.
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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.