Evidence map›Paper›PMID 23359592›Full record

ArticleThe Journal of infectious diseases2013

Intestinal epithelial restitution after TcdB challenge and recovery from Clostridium difficile infection in mice with alanyl-glutamine treatment.

Raphael S Rodrigues, Renato A C Oliveira, Yuesheng Li, Snjezana Zaja-Milatovic, Lourrany B Costa, Manuel B Braga Neto, Glynis L Kolling, Aldo A Lima, Richard L Guerrant, Cirle Alcantara Warren

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Reviewing theMicroorganisms · 2024
    Review
  4. Article
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  7. Clostridium difficile toxins or infection induce upregulation of adenosine receptors and IL-6 with early pro-inflammatory and late anti-inflammatory pattern.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    Article
  8. Alanyl-glutamine protects the intestinal barrier function in trained rats against the impact of acute exhaustive exercise.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    Article
  9. Review
  10. Review
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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

10 authors at 3 institutions in 2 countries.

Raphael S RodriguesBiomedicine Institute, Federal University of Ceará, Fortaleza, Brazil.
Renato A C Oliveira
Yuesheng Li
Snjezana Zaja-Milatovic
Lourrany B Costa
Manuel B Braga Neto
Glynis L Kolling
Aldo A Lima
Richard L Guerrant
Cirle Alcantara Warren
Universidade Federal do Ceará · BRUniversity of Virginia · USCenter for Global Health · US

Funding

Tailoring Novel Therapeutics for Emerging Drug-Resistant C. Difficile ColitisU01AI075526 · NIAID · UNIVERSITY OF VIRGINIA · PI GUERRANT, RICHARD L · 2007 to 2011
$3.6M
Global Infectious Disease Research Training Program at UVAD43TW006578 · FIC · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GUERRANT, RICHARD L · 2003 to 2018
$2.7M
FIC NIH HHS D43 TW0006578FIC NIH HHS D43 TW006578NIAID NIH HHS U01 AI075526
6 · The paper itself

Abstract

backgroundClostridium difficile is an anaerobic bacterium that causes antibiotic-associated diarrhea. It produces toxin A and toxin B (TcdB), which cause injury to the gut epithelium. Glutamine is a fundamental fuel for enterocytes, maintaining intestinal mucosal health. Alanyl-glutamine (AQ) is a highly soluble dipeptide derivative of glutamine. We studied whether administration of AQ ameliorates the effects of TcdB in the intestinal cells and improves the outcome of C. difficile infection in mice.

methodsWST-1 proliferation and cell-wounding-migration assays were assessed in IEC-6 cells exposed to TcdB, with or without AQ. Apoptosis and necrosis were assessed using Annexin V and flow cytometry. C57BL/6 mice were infected with VPI 10463 and treated with either vancomycin, AQ, or vancomycin with AQ. Intestinal tissues were collected for histopathologic analysis, apoptosis staining, and determination of myeloperoxidase activity.

resultsAQ increased proliferation in intestinal cells exposed to TcdB, improved migration at 24 and 48 hours, and reduced apoptosis in intestinal cells challenged with TcdB. Infected mice treated with vancomycin and AQ had better survival and histopathologic findings than mice treated with vancomycin alone.

conclusionsAQ may reduce intestinal mucosal injury in C. difficile-infected mice by partially reversing the effects of TcdB on enterocyte proliferation, migration, and apoptosis, thereby improving survival from C. difficile infection.

Indexed as

AnimalsApoptosisBacterial ProteinsBacterial ToxinsCell LineCell ProliferationClostridioides difficileClostridium InfectionsDipeptidesDisease Models, AnimalEnterocytesIntestinal MucosaMaleMiceMice, Inbred C57BLNecrosisalanylglutamineBacterial ProteinsBacterial ToxinsDipeptidestoxB protein, Clostridium difficileVancomycin

Identifiers

PMID23359592
PMCPMC3627196
OpenAlexW2158191464

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.