ArticlePLoS pathogens2005
Vibrio cholerae infection of Drosophila melanogaster mimics the human disease cholera.
Article in PLoS pathogens, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 115 citations in OpenAlex.
- Drosophila melanogaster as a model host for studying Pseudomonas aeruginosa feeding infection.Nature protocols · 2026Review
- A conserved, immune-regulated peritrophin promotes Vibrio cholerae colonization of the arthropod intestine.Nature communications · 2026Article
- The Drosophila G protein-coupled receptor, GulpR, is essential for lipid mobilization in response to nutrient-limitation.PLoS genetics · 2025Article
- Vibrio cholerae Invasion Dynamics of the Chironomid Host Are Strongly Influenced by Aquatic Cell Density and Can Vary by Strain.Microbiology spectrum · 2023Article
- Chromosomal Position of Ribosomal Protein Genes Affects Long-Term Evolution of Vibrio cholerae.mBio · 2023Article
- Advances in cholera research: from molecular biology to public health initiatives.Frontiers in microbiology · 2023Review
- Article
- New Insights into Vibrio cholerae Biofilms from Molecular Biophysics to Microbial Ecology.Advances in experimental medicine and biology · 2023Article
- Insights into Carbapenem Resistance inInternational journal of molecular sciences · 2022Review
- Vibrio cholerae high cell density quorum sensing activates the host intestinal innate immune response.Cell reports · 2022Article
- Article
- A mannose-sensing AraC-type transcriptional activator regulates cell-cell aggregation of Vibrio cholerae.NPJ biofilms and microbiomes · 2022Article
- Microbes affect gut epithelial cell composition through immune-dependent regulation of intestinal stem cell differentiation.Cell reports · 2022Article
- Animal models for dissecting Vibrio cholerae intestinal pathogenesis and immunity.Current opinion in microbiology · 2022Review
- Effects of intestinal microbiota on physiological metabolism and pathogenicity ofFrontiers in microbiology · 2022Review
- Article
- Review
- Methionine Availability in the Arthropod Intestine Is Elucidated through Identification of Vibrio cholerae Methionine Acquisition Systems.Applied and environmental microbiology · 2020Article
- Structural insights into the mechanism of oxidative activation of heme-free H-NOX from Vibrio cholerae.The Biochemical journal · 2020Article
- A Drosophila Model for Clostridium difficile Toxin CDT Reveals Interactions with Multiple Effector Pathways.iScience · 2020Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Cholera, the pandemic diarrheal disease caused by the gram-negative bacterium Vibrio cholerae, continues to be a major public health challenge in the developing world. Cholera toxin, which is responsible for the voluminous stools of cholera, causes constitutive activation of adenylyl cyclase, resulting in the export of ions into the intestinal lumen. Environmental studies have demonstrated a close association between V. cholerae and many species of arthropods including insects. Here we report the susceptibility of the fruit fly, Drosophila melanogaster, to oral V. cholerae infection through a process that exhibits many of the hallmarks of human disease: (i) death of the fly is dependent on the presence of cholera toxin and is preceded by rapid weight loss; (ii) flies harboring mutant alleles of either adenylyl cyclase, Gsalpha, or the Gardos K channel homolog SK are resistant to V. cholerae infection; and (iii) ingestion of a K channel blocker along with V. cholerae protects wild-type flies against death. In mammals, ingestion of as little as 25 mug of cholera toxin results in massive diarrhea. In contrast, we found that ingestion of cholera toxin was not lethal to the fly. However, when cholera toxin was co-administered with a pathogenic strain of V. cholerae carrying a chromosomal deletion of the genes encoding cholera toxin, death of the fly ensued. These findings suggest that additional virulence factors are required for intoxication of the fly that may not be essential for intoxication of mammals. Furthermore, we demonstrate for the first time the mechanism of action of cholera toxin in a whole organism and the utility of D. melanogaster as an accurate, inexpensive model for elucidation of host susceptibility to cholera.
Identifiers
What OpenQuestion holds
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.