ArticleJournal of cellular and molecular medicine2010
Bacterial intoxication evokes cellular senescence with persistent DNA damage and cytokine signalling.
Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 96 citations in OpenAlex.
- Host-Pathogen Interaction as a Driver of Cellular Senescence: Microbial Triggers and Host Response.International journal of molecular sciences · 2026Review
- Inflammation-responsive biomimetic hybrid nanovesicles reverse stem cell senescence by up-regulating SIRT1 to treat periodontitis.Journal of nanobiotechnology · 2026Article
- ATM and p53 in aging and cancer: a double-edged sword in genomic integrity.Biogerontology · 2025Review
- Combined In Situ Transcriptomic and Immunofluorescence to Assess the Effects on DNA Damage and Innate Immune Responses Induced by Bacterial Genotoxin in In Vivo Models.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Contribution of pks+Microorganisms · 2024Review
- Article
- The role of CYP-sEH derived lipid mediators in regulating mitochondrial biology and cellular senescence: implications for the aging heart.Frontiers in pharmacology · 2024Review
- Selective pks+ Escherichia coli strains induce cell cycle arrest and apoptosis in colon cancer cell line.World journal of microbiology & biotechnology · 2023Article
- Senescent Markers Expressed by Periodontal Ligament-Derived Stem Cells (PDLSCs) Harvested from Patients with Periodontitis Can Be Rejuvenated by RG108.Biomedicines · 2023Article
- Review
- Pathogen-driven cancers from a structural perspective: Targeting host-pathogen protein-protein interactions.Frontiers in oncology · 2023Review
- Genotoxin-producingFrontiers in immunology · 2023Article
- Delivery, structure, and function of bacterial genotoxins.Virulence · 2022Review
- Chronic exposure to Cytolethal Distending Toxin (CDT) promotes a cGAS-dependent type I interferon response.Cellular and molecular life sciences : CMLS · 2021Article
- Bacterial Toxins Are a Never-Ending Source of Surprises: From Natural Born Killers to Negotiators.Toxins · 2021Review
- The CDT of Helicobacter hepaticus induces pro-survival autophagy and nucleoplasmic reticulum formation concentrating the RNA binding proteins UNR/CSDE1 and P62/SQSTM1.PLoS pathogens · 2021Article
- Severe COVID-19 Lung Infection in Older People and Periodontitis.Journal of clinical medicine · 2021Review
- From DNA Damage to Cancer Progression: Potential Effects of Cytolethal Distending Toxin.Frontiers in immunology · 2021Review
- Cytolethal Distending Toxin Promotes Replicative Stress Leading to Genetic Instability Transmitted to Daughter Cells.Frontiers in cell and developmental biology · 2021Article
- Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytolethal distending toxins (CDTs) are proteins produced and secreted by facultative pathogenic strains of Gram-negative bacteria with potentially genotoxic effects. Mammalian cells exposed to CDTs undergo cell type-dependent cell-cycle arrest or apoptosis; however, the cell fate responses to such intoxication are mechanistically incompletely understood. Here we show that both normal and cancer cells (BJ, IMR-90 and WI-38 fibroblasts, HeLa and U2-OS cell lines) that survive the acute phase of intoxication by Haemophilus ducreyi CDT possess the hallmarks of cellular senescence. This characteristic phenotype included persistently activated DNA damage signalling (detected as 53BP1/gammaH2AX(+) foci), enhanced senescence-associated beta-galactosidase activity, expansion of promyelocytic leukaemia nuclear compartments and induced expression of several cytokines (especially interleukins IL-6, IL-8 and IL-24), overall features shared by cells undergoing replicative or premature cellular senescence. We conclude that analogous to oncogenic, oxidative and replicative stresses, bacterial intoxication represents another pathophysiological stimulus that induces premature senescence, an intrinsic cellular response that may mechanistically underlie the 'distended' morphology evoked by CDTs. Finally, the activation of the two anticancer barriers, apoptosis and cellular senescence, together with evidence of chromosomal aberrations (micronucleation) reported here, support the emerging genotoxic and potentially oncogenic effects of this group of bacterial toxins, and warrant further investigation of their role(s) in human disease.
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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.