ArticleMucosal immunology2017
Bacterial virulence factor inhibits caspase-4/11 activation in intestinal epithelial cells.
Article in Mucosal immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 76 citations in OpenAlex.
- GBP1 recruitment to actin-rich pedestals of extracellular Gram-negative bacteria promotes pyroptosis.The EMBO journal · 2026Article
- MAP4Ks drive cell death in response tomBio · 2026Article
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- The accessory type III secretion system effectors collectively shape intestinal inflammatory infection outcomes.Gut microbes · 2025Article
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- GBP1 recruitment to actin-rich pedestals induced by extracellular Gram negative bacteria promotes pyroptosis.bioRxiv : the preprint server for biology · 2025Article
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- A bacterial toxin co-opts caspase-3 to disable active gasdermin D and limit macrophage pyroptosis.Cell reports · 2024Article
- Article
- Article
- Gasdermin D independent canonical inflammasome responses cooperate with caspase-8 to establish host defense against gastrointestinal Citrobacter rodentium infection.Cell death & disease · 2023Article
- A bacterial autotransporter impairs innate immune responses by targeting the transcription factor TFE3.Nature communications · 2023Article
- Double-Edged Sword Effect of Pyroptosis: The Role of Caspase-1/-4/-5/-11 in Different Levels of Apical Periodontitis.Biomolecules · 2022Article
- Reprogramming of Cell Death Pathways by Bacterial Effectors as a Widespread Virulence Strategy.Infection and immunity · 2022Review
- Subtilase cytotoxin from Shiga-toxigeniciScience · 2022Article
- Mechanisms and Consequences of Noncanonical Inflammasome-Mediated Pyroptosis.Journal of molecular biology · 2022Review
- Article
- Caspase-4 and -5 Biology in the Pathogenesis of Inflammatory Bowel Disease.Frontiers in pharmacology · 2022Review
- Inhibition of PFKFB Preserves Intestinal Barrier Function in Sepsis by Inhibiting NLRP3/GSDMD.Oxidative medicine and cellular longevity · 2022Article
- Pyroptosis in development, inflammation and disease.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The human pathogen enteropathogenic Escherichia coli (EPEC), as well as the mouse pathogen Citrobacter rodentium, colonize the gut mucosa via attaching and effacing lesion formation and cause diarrheal diseases. EPEC and C. rodentium type III secretion system (T3SS) effectors repress innate immune responses and infiltration of immune cells. Inflammatory caspases such as caspase-1 and caspase-4/11 are crucial mediators of host defense and inflammation in the gut via their ability to process cytokines such as interleukin (IL)-1β and IL-18. Here we report that the effector NleF binds the catalytic domain of caspase-4 and inhibits its proteolytic activity. Following infection of intestinal epithelial cells (IECs) EPEC inhibited caspase-4 and IL-18 processing in an NleF-dependent manner. Depletion of caspase-4 in IECs prevented the secretion of mature IL-18 in response to infection with EPECΔnleF. NleF-dependent inhibition of caspase-11 in colons of mice prevented IL-18 secretion and neutrophil influx at early stages of C. rodentium infection. Neither wild-type C. rodentium nor C. rodentiumΔnleF triggered neutrophil infiltration or IL-18 secretion in Cas11 or Casp1/11-deficient mice. Thus, IECs have a key role in modulating early innate immune responses in the gut via a caspase-4/11-IL-18 axis, which is targeted by virulence factors encoded by enteric pathogens.
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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.