ArticleCellular and molecular life sciences : CMLS2021
Chronic exposure to Cytolethal Distending Toxin (CDT) promotes a cGAS-dependent type I interferon response.
Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Cytolethal distending toxin enhancesInfection and immunity · 2026Article
- ISG15 At the Crossroads of Innate Immunity and Host Survival in Response to Typhoid Toxin.Molecular microbiology · 2026Article
- Cytolethal Distending Toxin EnhancesbioRxiv : the preprint server for biology · 2026Article
- Gut microbiome-driven colorectal cancer via immune, metabolic, neural, and endocrine axes reprogramming.NPJ biofilms and microbiomes · 2026Review
- Typhoid toxin of Salmonella Typhi elicits host antimicrobial response during acute typhoid fever.EMBO molecular medicine · 2026Article
- Genome-scale CRISPR/Cas9 screening reveals the role ofmSphere · 2025Article
- Glucosinolates and Indole-3-carbinol fromIn silico pharmacology · 2024Article
- The footprint of gut microbiota in gallbladder cancer: a mechanistic review.Frontiers in cellular and infection microbiology · 2024Review
- The crucial regulatory role of type I interferon in inflammatory diseases.Cell & bioscience · 2023Review
- Beyond the List: Bioagent-Agnostic Signatures Could Enable a More Flexible and Resilient Biodefense Posture Than an Approach Based on Priority Agent Lists Alone.Pathogens (Basel, Switzerland) · 2021Article
- From DNA Damage to Cancer Progression: Potential Effects of Cytolethal Distending Toxin.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The Cytolethal Distending Toxin (CDT) is a bacterial genotoxin produced by pathogenic bacteria causing major foodborne diseases worldwide. CDT activates the DNA Damage Response and modulates the host immune response, but the precise relationship between these outcomes has not been addressed so far. Here, we show that chronic exposure to CDT in HeLa cells or mouse embryonic fibroblasts promotes a strong type I interferon (IFN) response that depends on the cytoplasmic DNA sensor cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase (cGAS) through the recognition of micronuclei. Indeed, despite active cell cycle checkpoints and in contrast to other DNA damaging agents, cells exposed to CDT reach mitosis where they accumulate massive DNA damage, resulting in chromosome fragmentation and micronucleus formation in daughter cells. These mitotic phenotypes are observed with CDT from various origins and in cancer or normal cell lines. Finally, we show that CDT exposure in immortalized normal colonic epithelial cells is associated to cGAS protein loss and low type I IFN response, implying that CDT immunomodulatory function may vary depending on tissue and cell type. Thus, our results establish a direct link between CDT-induced DNA damage, genetic instability and the cellular immune response that may be relevant in the context of natural infection associated to chronic inflammation or carcinogenesis.
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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.