ArticlePloS one2009
The Vibrio cholerae cytolysin promotes chloride secretion from intact human intestinal mucosa.
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 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Enigmatic roles ofJournal of bacteriology · 2025Review
- Systemic, Mucosal, and Memory Immune Responses following Cholera.Tropical medicine and infectious disease · 2021Review
- Expression of Hemolysin Is Regulated Under the Collective Actions of HapR, Fur, and HlyU inFrontiers in microbiology · 2018Article
- Transmission and Toxigenic Potential ofFrontiers in microbiology · 2018Article
- Quantifying Vibrio cholerae Enterotoxicity in a Zebrafish Infection Model.Applied and environmental microbiology · 2017Article
- Great cormorants (Phalacrocorax carbo) as potential vectors for the dispersal of Vibrio cholerae.Scientific reports · 2017Article
- Vibrio cholerae hemagglutinin(HA)/protease: An extracellular metalloprotease with multiple pathogenic activities.Toxicon : official journal of the International Society on Toxinology · 2016Review
- RAB11-mediated trafficking in host-pathogen interactions.Nature reviews. Microbiology · 2014Review
- Proteomic analysis of Vibrio cholerae outer membrane vesicles.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Bovine pericardium patch wrapping intestinal anastomosis improves healing process and prevents leakage in a pig model.PloS one · 2014Article
- Role of pore-forming toxins in bacterial infectious diseases.Microbiology and molecular biology reviews : MMBR · 2013Review
- Proteins secreted via the type II secretion system: smart strategies of Vibrio cholerae to maintain fitness in different ecological niches.PLoS pathogens · 2013Review
- Crystal structure of the Vibrio cholerae cytolysin heptamer reveals common features among disparate pore-forming toxins.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Horizontal gene transfers with or without cell fusions in all categories of the living matter.Advances in experimental medicine and biology · 2011Review
- Fish as reservoirs and vectors of Vibrio cholerae.PloS one · 2010Article
- Vibrio cholerae cytolysin causes an inflammatory response in human intestinal epithelial cells that is modulated by the PrtV protease.PloS one · 2009Article
- Memory T-cell responses to Vibrio cholerae O1 infection.Infection and immunity · 2009Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe pathogenicity of the Vibrio cholerae strains belonging to serogroup O1 and O139 is due to the production of virulence factors such as cholera toxin (CT) and the toxin-coregulated pilus (TCP). The remaining serogroups, which mostly lack CT and TCP, are more frequently isolated from aquatic environmental sources than from clinical samples; nevertheless, these strains have been reported to cause human disease, such as sporadic outbreaks of watery diarrhoea and inflammatory enterocolitis. This evidence suggested the possibility that other virulence factor(s) than cholera toxin might be crucial in the pathogenesis of Vibrio cholerae-induced diarrhoea, but their nature remains unknown. VCC, the hemolysin produced by virtually all Vibrio cholerae strains, has been proposed as a possible candidate, though a clear-cut demonstration attesting VCC as crucial in the pathogenesis of Vibrio cholerae-induced diarrhoea is still lacking. METHODOLOGY/PRINCIPAL
findingsElectrophysiological parameters and paracellular permeability of stripped human healthy colon tissues, obtained at subtotal colectomy, mounted in Ussing chamber were studied in the presence or absence of VCC purified from culture supernatants of V. cholerae O1 El Tor strain. Short circuit current (I(SC)) and transepithelial resistance (R(T)) were measured by a computerized voltage clamp system. The exposure of sigmoid colon specimens to 1 nM VCC resulted in an increase of I(SC) by 20.7%, with respect to the basal values, while R(T) was reduced by 12.3%. Moreover, increase in I(SC) was abolished by bilateral Cl(-) reduction. CONCLUSION/SIGNIFICANCE: Our results demonstrate that VCC, by forming anion channels on the apical membrane of enterocytes, triggers an outward transcellular flux of chloride. Such an ion movement, associated with the outward movement of Na(+) and water, might be responsible for the diarrhoea caused by the non-toxigenic strains of Vibrio cholerae.
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