Evidence map›Paper›PMID 26999202›Full record

ReviewToxins2016

Clostridium perfringens Enterotoxin: Action, Genetics, and Translational Applications.

John C Freedman, Archana Shrestha, Bruce A McClane

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 1 pooled it
14.9field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 1 synthesis or guideline pooled it, 208 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Type A and DFrontiers in cellular and infection microbiology · 2026
    Article
  9. A novel broad-spectrum phage lysin CP02 for biocontrol ofCurrent research in food science · 2026
    Article
  10. Article
  11. Sporulation Abilities and Heat Resistance ofFoods (Basel, Switzerland) · 2025
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Characterization ofAntibiotics (Basel, Switzerland) · 2025
    Article
  20. Deadly Diarrhea Caused by Co-Infection ofInfection and drug resistance · 2025
    Article

51 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

3 authors at 1 institution in 1 country.

John C FreedmanDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA. jcf63@pitt.edu.
Archana ShresthaDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA. ars139@pitt.edu.
Bruce A McClaneDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA. bamcc@pitt.edu.
University of Pittsburgh · US

Funding

MECHANISMS OF ACTION OF C PERFRINGENS EXTEROTOXINR01AI019844 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MC CLANE, BRUCE A · 1985 to 2024
$5.4M
Immunology of Infectious DiseaseT32AI060525 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JoAnne L. Flynn · 2005 to 2026
$5.3M
NIAID NIH HHS 5T32AI060525-10NIAID NIH HHS AI0198844-33NIAID NIH HHS R01 AI019844NIAID NIH HHS T32 AI060525
6 · The paper itself

Abstract

Clostridium perfringens enterotoxin (CPE) is responsible for causing the gastrointestinal symptoms of several C. perfringens food- and nonfood-borne human gastrointestinal diseases. The enterotoxin gene (cpe) is located on either the chromosome (for most C. perfringens type A food poisoning strains) or large conjugative plasmids (for the remaining type A food poisoning and most, if not all, other CPE-producing strains). In all CPE-positive strains, the cpe gene is strongly associated with insertion sequences that may help to assist its mobilization and spread. During disease, CPE is produced when C. perfringens sporulates in the intestines, a process involving several sporulation-specific alternative sigma factors. The action of CPE starts with its binding to claudin receptors to form a small complex; those small complexes then oligomerize to create a hexameric prepore on the membrane surface. Beta hairpin loops from the CPE molecules in the prepore assemble into a beta barrel that inserts into the membrane to form an active pore that enhances calcium influx, causing cell death. This cell death results in intestinal damage that causes fluid and electrolyte loss. CPE is now being explored for translational applications including cancer therapy/diagnosis, drug delivery, and vaccination.

Indexed as

EnterotoxinsAnimalsGastrointestinal DiseasesHumansVaccinesenterotoxin, ClostridiumEnterotoxinsVaccinesclaudinsClostridium perfringensenterotoxinpore-forming toxinsporulationtight junctions

Identifiers

PMID26999202
PMCPMC4810218
OpenAlexW2302192047

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.