Evidence map›Paper›PMID 21454368›Full record

ArticleMicrobiology (Reading, England)2011

A novel antimicrobial peptide significantly enhances acid-induced killing of Shiga toxin-producing Escherichia coli O157 and non-O157 serotypes.

M Lino, J V Kus, S L Tran, Z Naqvi, B Binnington, S D Goodman, A M Segall, D Barnett Foster

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Microbiology (Reading, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. EnterohemorrhagicInternational journal of molecular sciences · 2022
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Antimicrobial peptides and colitis.Current pharmaceutical design · 2013
    Review
  8. Article
  9. Article
  10. 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

8 authors at 4 institutions in 2 countries.

M LinoDepartment of Chemistry and Biology, Ryerson University, Toronto, ON, Canada.
J V KusDepartment of Chemistry and Biology, Ryerson University, Toronto, ON, Canada.
S L TranDepartment of Chemistry and Biology, Ryerson University, Toronto, ON, Canada.
Z NaqviDepartment of Chemistry and Biology, Ryerson University, Toronto, ON, Canada.
B BinningtonMolecular Structure and Function, Hospital for Sick Children, Toronto, ON, Canada.
S D GoodmanDivision of Biomedical Sciences, Herman Ostrow School of Dentistry of the University of Southern California, USA.
A M SegallDepartment of Biology, Center for Microbial Sciences and Molecular Biology Institute, San Diego State University, USA.
D Barnett FosterMolecular Structure and Function, Hospital for Sick Children, Toronto, ON, Canada.
Toronto Metropolitan University · CAHospital for Sick Children · CASan Diego State University · USUniversity of Southern California · US

Funding

Novel antibiotics that trap Holliday junctionsR01AI058253 · NIAID · SAN DIEGO STATE UNIVERSITY · PI SEGALL, ANCA MARA · 2004 to 2008
$2.3M
NIAID NIH HHS R01 AI058253PHS HHS R01-058253A1
6 · The paper itself

Abstract

Shiga toxin-producing Escherichia coli (STEC) colonizes the human intestine, causing haemorrhagic colitis and haemolytic uraemic syndrome (HUS). Treatment options are limited to intravenous fluids in part because sublethal doses of some antibiotics have been shown to stimulate increased toxin release and enhance the risk of progression to HUS. Preventative antimicrobial agents, especially those that build on the natural antimicrobial action of the host defence, may provide a better option. In order to survive the acid stress of gastric passage, STEC is equipped with numerous acid resistance and DNA repair mechanisms. Inhibition of acid-induced DNA repair may offer a strategy to target survival of ingested STEC. We report here that brief pretreatment with a novel antimicrobial peptide, which was previously shown to inhibit bacterial DNA repair, significantly and profoundly reduces survival of acid-stressed O157 : H7 and non-O157 : H7 STEC seropathotypes that are highly associated with HUS. Reduction in survival rates of STEC range from 3 to 5 log. We also show that peptide/acid treatment results in little or no increase in toxin production, thereby reducing the risk of progression to HUS. This study identifies the peptide wrwycr as a potential new candidate for a preventative antimicrobial for STEC infection.

Indexed as

AnimalsAntimicrobial Cationic PeptidesChlorocebus aethiopsEscherichia coliEscherichia coli O157Hemolytic-Uremic SyndromeHumansHydrochloric AcidHydrogen-Ion ConcentrationMicrobial Sensitivity TestsSerotypingShiga-Toxigenic Escherichia coliShiga ToxinsVero CellsAntimicrobial Cationic PeptidesHydrochloric AcidShiga Toxins

Identifiers

PMID21454368
PMCPMC3167915
OpenAlexW2097272516

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.