Evidence map›Paper›PMID 23811846›Full record

ArticleGut microbes

Role of host xanthine oxidase in infection due to enteropathogenic and Shiga-toxigenic Escherichia coli.

John K Crane

Abstract readComment
In one paragraph

Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

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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

26 citing papers in PubMed.

  1. Article
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  16. Characteristic alterations of gut microbiota in uncontrolled gout.Journal of microbiology (Seoul, Korea) · 2022
    Article
  17. Article
  18. Review
  19. Article
  20. Impact ofNutrients · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

John K CraneDivision of Infectious Diseases; University at Buffalo; Buffalo, NY USA.

Funding

Enhancing Host Intestinal Defenses against Enteropathogenic and Shiga toxigenic ER21AI102212 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI CRANE, JOHN K. · 2012 to 2013
$415k
NIAID NIH HHS R21 AI 102212NIAID NIH HHS R21 AI102212
6 · The paper itself

Abstract

Xanthine oxidase (XO) has been recognized as an important host defense enzyme for decades. In our recent study in Infection and Immunity, we found that enteropathogenic and Shiga-toxigenic E. coli (EPEC and STEC) were far more resistant to killing by the XO pathway than laboratory E. coli strains used in the past. Although XO plus hypoxanthine substrate rarely generated enough H 2O 2 to kill EPEC and STEC, the pathogens were able to sense the H2O2 and react to it with an increase in expression of virulence factors, most notably Shiga toxin (Stx). H 2O 2 produced by XO also triggered a chloride secretory response in T84 cell monolayers studied in the Ussing chamber. Adding exogenous XO plus its substrate in vivo did not decrease the number of STEC bacteria recovered from ligated intestinal loops, but instead appeared to worsen the infection and increased the amount of Stx2 toxin produced. XO plus hypoxanthine also increases the ability of Stx2 to translocate across intestinal monolayers. With regard to EPEC and STEC, the role of XO appears more complex and subtle than what has been reported in the past, since XO also plays a role in host-pathogen signaling, in regulating virulence in pathogens, in Stx production and in toxin translocation. Uric acid produced by XO may also be in itself an immune modulator in the intestinal tract.

Indexed as

Host-Pathogen InteractionsAnimalsEnteropathogenic Escherichia coliEscherichia coli InfectionsHumansShiga-Toxigenic Escherichia coliXanthine OxidaseXanthine Oxidasebiomarkerdiarrheal diseaseenteropathogenicpurinergic signalingShiga toxinsuncanny valleyuric acid

Identifiers

PMID23811846
PMCPMC3839983

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Registered trials

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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.