ArticlePloS one2010
Vibrio cholerae hemolysin is required for lethality, developmental delay, and intestinal vacuolation in Caenorhabditis elegans.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Enigmatic roles ofJournal of bacteriology · 2025Review
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- Unveiling potential virulence determinants inMicrobiology spectrum · 2024Article
- Novel Nematode-Killing Protein-1 (Nkp-1) from a Marine Epiphytic BacteriumBiomedicines · 2021Article
- 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
- Vibrio cholerae Infection Induces Strain-Specific Modulation of the Zebrafish Intestinal Microbiome.Infection and immunity · 2021Article
- Dissecting serotype-specific contributions to live oral cholera vaccine efficacy.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Cell Death Signaling Pathway Induced by Cholix Toxin, a Cytotoxin and eEF2 ADP-Ribosyltransferase Produced byToxins · 2020Review
- Combining microfluidics and RNA-sequencing to assess the inducible defensome of a mushroom against nematodes.BMC genomics · 2019Article
- Review
- Molecular insights into Vibrio cholerae's intra-amoebal host-pathogen interactions.Nature communications · 2018Article
- Expression of Hemolysin Is Regulated Under the Collective Actions of HapR, Fur, and HlyU inFrontiers in microbiology · 2018Article
- The Nematode Caenorhabditis Elegans - A Versatile In Vivo Model to Study Host-microbe Interactions.Journal of visualized experiments : JoVE · 2017Article
- An Enterotoxin-Like Binary Protein from Pseudomonas protegens with Potent Nematicidal Activity.Applied and environmental microbiology · 2017Article
- Quantifying Vibrio cholerae Enterotoxicity in a Zebrafish Infection Model.Applied and environmental microbiology · 2017Article
- Vibrio cholerae hemagglutinin(HA)/protease: An extracellular metalloprotease with multiple pathogenic activities.Toxicon : official journal of the International Society on Toxinology · 2016Review
- Oligonol promotes anti-aging pathways via modulation of SIRT1-AMPK-Autophagy Pathway.Nutrition research and practice · 2016Article
- Signaling beyond Punching Holes: Modulation of Cellular Responses by Vibrio cholerae Cytolysin.Toxins · 2015Review
- Nontoxigenic Vibrio cholerae non-O1/O139 isolate from a case of human gastroenteritis in the U.S. Gulf Coast.Journal of clinical microbiology · 2015Article
- Proteomic analysis of Vibrio cholerae outer membrane vesicles.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCholera toxin (CT) and toxin-co-regulated pili (TCP) are the major virulence factors of Vibrio cholerae O1 and O139 strains that contribute to the pathogenesis of disease during devastating cholera pandemics. However, CT and TCP negative V. cholerae strains are still able to cause severe diarrheal disease in humans through mechanisms that are not well understood. METHODOLOGY/PRINCIPAL
findingsTo determine the role of other virulence factors in V. cholerae pathogenesis, we used a CT and TCP independent infection model in the nematode Caenorhabditis elegans and identified the hemolysin A (hlyA) gene as a factor responsible for animal death and developmental delay. We demonstrated a correlation between the severity of infection in the nematode and the level of hemolytic activity in the V. cholerae biotypes. At the cellular level, V. cholerae infection induces formation of vacuoles in the intestinal cells in a hlyA dependent manner, consistent with the previous in vitro observations. CONCLUSIONS/SIGNIFICANCE: Our data strongly suggest that HlyA is a virulence factor in C. elegans infection leading to lethality and developmental delay presumably through intestinal cytopathic changes.
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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.