ArticlePLoS pathogens2017
Vibrio cholerae ensures function of host proteins required for virulence through consumption of luminal methionine sulfoxide.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- A conserved, immune-regulated peritrophin promotes Vibrio cholerae colonization of the arthropod intestine.Nature communications · 2026Article
- An integrated Msr-antioxidase-host gene circuit maintains redox homeostasis in legume-rhizobium symbiosis.Frontiers in plant science · 2026Article
- Insect Lipidomics: Advances, Applications, and Physiological Insights.Advances in experimental medicine and biology · 2026Review
- Advances in cholera research: from molecular biology to public health initiatives.Frontiers in microbiology · 2023Review
- Vibrio cholerae high cell density quorum sensing activates the host intestinal innate immune response.Cell reports · 2022Article
- Animal models for dissecting Vibrio cholerae intestinal pathogenesis and immunity.Current opinion in microbiology · 2022Review
- Metabolic Alterations in Shrimp Stomach During Acute Hepatopancreatic Necrosis Disease and Effects of Taurocholate onFrontiers in microbiology · 2021Article
- Methionine Availability in the Arthropod Intestine Is Elucidated through Identification of Vibrio cholerae Methionine Acquisition Systems.Applied and environmental microbiology · 2020Article
- Microbial Control of Intestinal Homeostasis via Enteroendocrine Cell Innate Immune Signaling.Trends in microbiology · 2020Review
- Article
- Lipid Droplets: A Significant but Understudied Contributor of Host⁻Bacterial Interactions.Cells · 2019Review
- Host-Microbe-Pathogen Interactions: A Review ofFrontiers in immunology · 2019Review
- Shedding Light on Specificity: Population Genomic Structure of a Symbiosis Between a Coral Reef Fish and Luminous Bacterium.Frontiers in microbiology · 2019Article
- Modulation of CrbS-Dependent Activation of the Acetate Switch in Vibrio cholerae.Journal of bacteriology · 2018Article
- A Putative Acetylation System in Vibrio cholerae Modulates Virulence in Arthropod Hosts.Applied and environmental microbiology · 2018Article
- The Role of Methionine Sulfoxide Reductases in Oxidative Stress Tolerance and Virulence ofAntioxidants (Basel, Switzerland) · 2018Review
- Article
- Activation of Vibrio cholerae quorum sensing promotes survival of an arthropod host.Nature microbiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Vibrio cholerae is a diarrheal pathogen that induces accumulation of lipid droplets in enterocytes, leading to lethal infection of the model host Drosophila melanogaster. Through untargeted lipidomics, we provide evidence that this process is the product of a host phospholipid degradation cascade that induces lipid droplet coalescence in enterocytes. This infection-induced cascade is inhibited by mutation of the V. cholerae glycine cleavage system due to intestinal accumulation of methionine sulfoxide (MetO), and both dietary supplementation with MetO and enterocyte knock-down of host methionine sulfoxide reductase A (MsrA) yield increased resistance to infection. MsrA converts both free and protein-associated MetO to methionine. These findings support a model in which dietary MetO competitively inhibits repair of host proteins by MsrA. Bacterial virulence strategies depend on functional host proteins. We propose a novel virulence paradigm in which an intestinal pathogen ensures the repair of host proteins essential for pathogenesis through consumption of dietary MetO.
Indexed as
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.