Evidence map›Paper›PMID 25569153›Full record

ArticlePLoS pathogens2015

The molecular basis for control of ETEC enterotoxin expression in response to environment and host.

James R J Haycocks, Prateek Sharma, Anne M Stringer, Joseph T Wade, David C Grainger

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
6.0field-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

33 citing papers in PubMed, 55 citations in OpenAlex.

  1. EnterotoxigenicProceedings of the National Academy of Sciences of the United States of America · 2018
    Trial
  2. The divergentMicrobiology (Reading, England) · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Augmented Enterocyte Damage DuringFrontiers in cellular and infection microbiology · 2022
    Article
  15. DissectingJournal of bacteriology · 2021
    Article
  16. Article
  17. Strain-specific transcriptional and posttranscriptional regulation of heat-labile toxin expression by enterotoxigenic Escherichia coli.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2020
    Article
  18. Article
  19. Review
  20. Article
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

5 authors at 3 institutions in 2 countries.

James R J HaycocksInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Prateek SharmaInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Anne M StringerWadsworth Center, New York State Department of Health, Albany, New York, United States of America.
Joseph T WadeWadsworth Center, New York State Department of Health, Albany, New York, United States of America; Department of Biomedical Sciences, School of Public Health, University at Albany, SUNY, Albany, New York, United States of America.
David C GraingerInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
University of Birmingham · GBNew York State Department of Health · USWadsworth Center · US

Funding

Wellcome TrustWellcome Trust WT085092MA
6 · The paper itself

Abstract

Enterotoxigenic Escherichia coli (ETEC) cause severe diarrhoea in humans and neonatal farm animals. Annually, 380,000 human deaths, and multi-million dollar losses in the farming industry, can be attributed to ETEC infections. Illness results from the action of enterotoxins, which disrupt signalling pathways that manage water and electrolyte homeostasis in the mammalian gut. The resulting fluid loss is treated by oral rehydration. Hence, aqueous solutions of glucose and salt are ingested by the patient. Given the central role of enterotoxins in disease, we have characterised the regulatory trigger that controls toxin production. We show that, at the molecular level, the trigger is comprised of two gene regulatory proteins, CRP and H-NS. Strikingly, this renders toxin expression sensitive to both conditions encountered on host cell attachment and the components of oral rehydration therapy. For example, enterotoxin expression is induced by salt in an H-NS dependent manner. Furthermore, depending on the toxin gene, expression is activated or repressed by glucose. The precise sensitivity of the regulatory trigger to glucose differs because of variations in the regulatory setup for each toxin encoding gene.

Indexed as

EnvironmentAnimalsBase SequenceCaco-2 CellsEnterotoxigenic Escherichia coliEnterotoxinsEscherichia coli InfectionsGene-Environment InteractionGene Expression Regulation, BacterialHost-Pathogen InteractionsHumansMiceMice, Inbred BALB CMolecular Sequence DataEnterotoxins

Identifiers

PMID25569153
PMCPMC4287617
OpenAlexW1997882630

What OpenQuestion holds

Textmetadata
LicenceCC0
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.