Evidence map›Paper›PMID 17698573›Full record

ArticleInfection and immunity2007

Hemolysin and the multifunctional autoprocessing RTX toxin are virulence factors during intestinal infection of mice with Vibrio cholerae El Tor O1 strains.

Verena Olivier, G Kenneth Haines, Yanping Tan, Karla J Fullner Satchell

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
7.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 99 citations in OpenAlex.

  1. Actuation of CRP activating region 3 by formylation modulates theProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Enigmatic roles ofJournal of bacteriology · 2025
    Review
  3. Science advances · 2025
    Article
  4. Biantennary N-glycans As Receptors for MARTX Toxins inbioRxiv : the preprint server for biology · 2024
    Article
  5. Article
  6. Article
  7. Cholera Dynamics and the Emergence of Pandemic Vibrio cholerae.Advances in experimental medicine and biology · 2023
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. TheScience signaling · 2020
    Article
  14. Article
  15. Indole Inhibits ToxR Regulon Expression inInfection and immunity · 2019
    Article
  16. Review
  17. El Tor BiotypeFrontiers in immunology · 2019
    Article
  18. Article
  19. Article
  20. Article

4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Verena OlivierDepartment of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
G Kenneth Haines
Yanping Tan
Karla J Fullner Satchell
Northwestern University · US

Funding

Genetic and biochemical study ov V. cholerase RTX toxinR01AI051490 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SATCHELL, KARLA J F · 2003 to 2012
$3.3M
NIAID NIH HHS AI051490NIAID NIH HHS R01 AI051490
6 · The paper itself

Abstract

The seventh cholera pandemic that started in 1961 was caused by Vibrio cholerae O1 strains of the El Tor biotype. These strains produce the pore-forming toxin hemolysin, a characteristic used clinically to distinguish classical and El Tor biotypes. Even though extensive in vitro data on the cytolytic activities of hemolysin exist, the connection of hemolysin to virulence in vivo is not well characterized. To study the contribution of hemolysin and other accessory toxins to pathogenesis, we utilized the model of intestinal infection in adult mice sensitive to the actions of accessory toxins. In this study, we showed that 4- to 6-week-old streptomycin-fed C57BL/6 mice were susceptible to intestinal infection with El Tor strains, which caused rapid death at high doses. Hemolysin had the predominant role in lethality, with a secondary contribution by the multifunctional autoprocessing RTX (MARTX) toxin. Cholera toxin and hemagglutinin/protease did not contribute to lethality in this model. Rapid death was not caused by increased dissemination due to a damaged epithelium since the numbers of CFU recovered from spleens and livers 6 h after infection did not differ between mice inoculated with hemolysin-expressing strains and those infected with non-hemolysin-expressing strains. Although accessory toxins were linked to virulence, a strain defective in the production of accessory toxins was still immunogenic since mice immunized with a multitoxin-deficient strain were protected from a subsequent lethal challenge with the wild type. These data suggest that hemolysin and MARTX toxin contribute to vaccine reactogenicity but that the genes for these toxins can be deleted from vaccine strains without affecting vaccine efficacy.

Indexed as

AnimalsBacterial ProteinsBacterial ToxinsBacterial VaccinesCholeraCholera ToxinColony Count, MicrobialFemaleHemolysin ProteinsIntestine, SmallLiverMetalloendopeptidasesMiceMice, Inbred C57BLSpleenSurvival AnalysisBacterial ProteinsBacterial ToxinsBacterial VaccinesCholera Toxinhemagglutinin-proteaseHemolysin ProteinshlyA protein, Vibrio choleraeMetalloendopeptidasesRtxA protein, Vibrio choleraeVirulence Factors

Identifiers

PMID17698573
PMCPMC2044521
OpenAlexW2097456855

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.