ArticleProceedings of the National Academy of Sciences of the United States of America2007
Protective role of autophagy against Vibrio cholerae cytolysin, a pore-forming toxin from V. cholerae.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 3 of them syntheses that pooled it.
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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
89 citing papers in PubMed, 3 syntheses or guidelines pooled it, 177 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
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- Bergeyella cardium variant induces a unique cytoplasmic vacuolization cell death floatptosis in macrophage.Cell discovery · 2025Article
- Genomic Analysis and Virulence Features of Vibrio cholerae Non-O1/Non-O139 Harbouring CARB-Type β-Lactamases From Freshwater Bodies, Argentina.Environmental microbiology reports · 2025Article
- Enigmatic roles ofJournal of bacteriology · 2025Review
- Andrographolide derivative CX-10 alleviates ulcerative colitis by modulating autophagy and cellular stress.Journal of clinical biochemistry and nutrition · 2025Article
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- Vibrio cholerae cytolysin induces pro-inflammatory and death signals through novel TLR assembly.PLoS pathogens · 2025Article
- Public health aspects ofEFSA journal. European Food Safety Authority · 2024Article
- Plasma membrane repair empowers the necrotic survivors as innate immune modulators.Seminars in cell & developmental biology · 2024Review
- Breaking the cellular defense: the role of autophagy evasion inFrontiers in cellular and infection microbiology · 2024Article
- Phenol-Soluble Modulin α3 Stimulates Autophagy in HaCaT Keratinocytes.Biomedicines · 2023Article
- Aminopeptidase MNP-1 triggers intestine protease production by activating daf-16 nuclear location to degrade pore-forming toxins in Caenorhabditis elegans.PLoS pathogens · 2023Article
- Transcriptional Activation of a Pro-Inflammatory Response (NF-κB, AP-1, IL-1β) by theInternational journal of molecular sciences · 2023Article
- How autophagy, a potential therapeutic target, regulates intestinal inflammation.Frontiers in immunology · 2023Review
- ARF GTPases activate Salmonella effector SopF to ADP-ribosylate host V-ATPase and inhibit endomembrane damage-induced autophagy.Nature structural & molecular biology · 2022Article
- Interactions of Autophagy and the Immune System in Health and Diseases.Autophagy reports · 2022Article
- Autophagy in major human diseases.The EMBO journal · 2021Review
- Beyond pore formation: reorganization of the plasma membrane induced by pore-forming proteins.Cellular and molecular life sciences : CMLS · 2021Review
29 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is the unique, regulated mechanism for the degradation of organelles. This intracellular process acts as a prosurvival pathway during cell starvation or stress and is also involved in cellular response against specific bacterial infections. Vibrio cholerae is a noninvasive intestinal pathogen that has been studied extensively as the causative agent of the human disease cholera. V. cholerae illness is produced primarily through the expression of a potent toxin (cholera toxin) within the human intestine. Besides cholera toxin, this bacterium secretes a hemolytic exotoxin termed V. cholerae cytolysin (VCC) that causes extensive vacuolation in epithelial cells. In this work, we explored the relationship between the vacuolation caused by VCC and the autophagic pathway. Treatment of cells with VCC increased the punctate distribution of LC3, a feature indicative of autophagosome formation. Moreover, VCC-induced vacuoles colocalized with LC3 in several cell lines, including human intestinal Caco-2 cells, indicating the interaction of the large vacuoles with autophagic vesicles. Electron microscopy analysis confirmed that the vacuoles caused by VCC presented hallmarks of autophagosomes. Additionally, biochemical evidence demonstrated the degradative nature of the VCC-generated vacuoles. Interestingly, autophagy inhibition resulted in decreased survival of Caco-2 cells upon VCC intoxication. Also, VCC failed to induce vacuolization in Atg5-/- cells, and the survival response of these cells against the toxin was dramatically impaired. These results demonstrate that autophagy acts as a cellular defense pathway against secreted bacterial toxins.
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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.