ArticlePloS one2009
Vibrio cholerae cytolysin causes an inflammatory response in human intestinal epithelial cells that is modulated by the PrtV protease.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- HapA protease targets PAR-1/2 to modulate ERK signalling and reduce cancer cell viability.Cell death discovery · 2025Article
- Enigmatic roles ofJournal of bacteriology · 2025Review
- Multi-cohort metagenomics reveals strain functional heterogeneity and demonstrates fecal microbial load correction improves colorectal cancer diagnostic models.Frontiers in microbiology · 2025Article
- Elucidation of cellular signaling mechanism involved inInfectious medicine · 2024Article
- The Vibrio cholerae Type Six Secretion System Is Dispensable for Colonization but Affects Pathogenesis and the Structure of Zebrafish Intestinal Microbiome.Infection and immunity · 2021Article
- Immune-Mediated Aggravation of theInternational journal of molecular sciences · 2021Article
- Vibrio cholerae derived outer membrane vesicles modulate the inflammatory response of human intestinal epithelial cells by inducing microRNA-146a.Scientific reports · 2019Article
- Environmental role of pathogenic traits inJournal of bacteriology · 2018Article
- Involvement of CYP1B1 in interferon γ-induced alterations of epithelial barrier integrity.British journal of pharmacology · 2018Article
- Analysis of the Human Mucosal Response to Cholera Reveals Sustained Activation of Innate Immune Signaling Pathways.Infection and immunity · 2018Article
- A Novel Role ofFrontiers in cellular and infection microbiology · 2017Article
- Article
- Cytotoxic and Inflammatory Responses Induced by Outer Membrane Vesicle-Associated Biologically Active Proteases from Vibrio cholerae.Infection and immunity · 2016Article
- Signaling beyond Punching Holes: Modulation of Cellular Responses by Vibrio cholerae Cytolysin.Toxins · 2015Review
- Genomics of immune response to typhoid and cholera vaccines.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Article
- Outer Membrane Vesicle-Mediated Export of Processed PrtV Protease from Vibrio cholerae.PloS one · 2015Article
- Vibrio cholerae-induced inflammation in the neonatal mouse cholera model.Infection and immunity · 2014Article
- Outer membrane vesicles mediate transport of biologically active Vibrio cholerae cytolysin (VCC) from V. cholerae strains.PloS one · 2014Article
- Pathogenesis of human enterovirulent bacteria: lessons from cultured, fully differentiated human colon cancer cell lines.Microbiology and molecular biology reviews : MMBR · 2013Review
- Genomic correlates of variability in immune response to an oral cholera vaccine.European journal of human genetics : EJHG · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundVibrio cholerae is the causal intestinal pathogen of the diarrheal disease cholera. It secretes the protease PrtV, which protects the bacterium from invertebrate predators but reduces the ability of Vibrio-secreted factor(s) to induce interleukin-8 (IL-8) production by human intestinal epithelial cells. The aim was to identify the secreted component(s) of V. cholerae that induces an epithelial inflammatory response and to define whether it is a substrate for PrtV. METHODOLOGY/PRINCIPAL
findingsCulture supernatants of wild type V. cholerae O1 strain C6706, its derivatives and pure V. cholerae cytolysin (VCC) were analyzed for the capacity to induce changes in cytokine mRNA expression levels, IL-8 and tumor necrosis factor-alpha (TNF-alpha) secretion, permeability and cell viability when added to the apical side of polarized tight monolayer T84 cells used as an in vitro model for human intestinal epithelium. Culture supernatants were also analyzed for hemolytic activity and for the presence of PrtV and VCC by immunoblot analysis. CONCLUSIONS/SIGNIFICANCE: We suggest that VCC is capable of causing an inflammatory response characterized by increased permeability and production of IL-8 and TNF-alpha in tight monolayers. Pure VCC at a concentration of 160 ng/ml caused an inflammatory response that reached the magnitude of that caused by Vibrio-secreted factors, while higher concentrations caused epithelial cell death. The inflammatory response was totally abolished by treatment with PrtV. The findings suggest that low doses of VCC initiate a local immune defense reaction while high doses lead to intestinal epithelial lesions. Furthermore, VCC is indeed a substrate for PrtV and PrtV seems to execute an environment-dependent modulation of the activity of VCC that may be the cause of V. cholerae reactogenicity.
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