ArticleMedical microbiology and immunology2008
Pro-inflammatory feedback activation cycle evoked by attack of Vibrio cholerae cytolysin on human neutrophil granulocytes.
Article in Medical microbiology and immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Vibrio cholerae cytolysin induces pro-inflammatory and death signals through novel TLR assembly.PLoS pathogens · 2025Article
- The Relationship between Glycan Binding and Direct Membrane Interactions in Vibrio cholerae Cytolysin, a Channel-forming Toxin.The Journal of biological chemistry · 2015Article
- Vibrio cholerae cytolysin recognizes the heptasaccharide core of complex N-glycans with nanomolar affinity.Journal of molecular biology · 2013Article
- Vibrio cholerae evades neutrophil extracellular traps by the activity of two extracellular nucleases.PLoS pathogens · 2013Article
- Neutrophils are essential for containment of Vibrio cholerae to the intestine during the proinflammatory phase of infection.Infection and immunity · 2012Article
- Neutrophil extracellular traps directly induce epithelial and endothelial cell death: a predominant role of histones.PloS one · 2012Article
- 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
- The clinical value of neutrophil extracellular traps.Medical microbiology and immunology · 2009Review
- Successful small intestine colonization of adult mice by Vibrio cholerae requires ketamine anesthesia and accessory toxins.PloS one · 2009Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vibrio cholerae cytolysin (VCC) is a pore-forming toxin that is secreted in precursor form (pro-VCC) and requires proteolytic cleavage in order to attain membrane-permeabilizing properties. Pro-VCC can be activated both in solution and membrane-bound state. Processing of membrane-bound pro-VCC can in turn be achieved through the action of both cell-associated and soluble proteases. The current investigation describes the interaction of VCC with human neutrophil granulocytes. It is shown that pro-VCC binds to these cells and is cleaved by cell-bound serine proteases. Membrane permeabilization leads to granulocyte activation, as witnessed by the generation of reactive oxygen metabolites and liberation of granule constituents. A mutant toxin with unaltered binding properties but devoid of pore-forming activity did not elicit these effects. The secreted proteases cleave and activate further bound- and non-bound pro-VCC. A positive feedback loop is thus created that results in enhanced cytotoxicity towards both the targeted granulocytes and towards bystander cells that are not primarily killed by the protoxin. Thus, activation of neutrophil granulocytes by VCC fuels a positive feedback cycle that will cripple immune defence, augment inflammation, and enhance the cytotoxic action of the toxin on neighbouring tissue cells.
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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.