Evidence map›Paper›PMID 28368463›Full record

ArticleThe Journal of infectious diseases2017

Enteric Helminths Promote Salmonella Coinfection by Altering the Intestinal Metabolome.

Lisa A Reynolds, Stephen A Redpath, Sophie Yurist-Doutsch, Navkiran Gill, Eric M Brown, Joris van der Heijden, Tara P Brosschot, Jun Han, Natalie C Marshall, Sarah E Woodward and 4 more

Abstract read
In one paragraph

Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

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

43 citing papers in PubMed.

  1. Article
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  6. ConcurrentmSphere · 2024
    Article
  7. Review
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  15. Article
  16. Review
  17. Article
  18. Lectin-Mediated Bacterial Modulation by the Intestinal NematodeInternational journal of molecular sciences · 2021
    Article
  19. Infection withPathogens (Basel, Switzerland) · 2021
    Article
  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

14 authors.

Lisa A ReynoldsMichael Smith Laboratories, University of British Columbia, Vancouver.
Stephen A RedpathDepartment of Microbiology and Immunology, University of British Columbia, Vancouver.
Sophie Yurist-DoutschMichael Smith Laboratories, University of British Columbia, Vancouver.
Navkiran GillMichael Smith Laboratories, University of British Columbia, Vancouver.
Eric M BrownMichael Smith Laboratories, University of British Columbia, Vancouver.
Joris van der HeijdenMichael Smith Laboratories, University of British Columbia, Vancouver.
Tara P BrosschotMichael Smith Laboratories, University of British Columbia, Vancouver.
Jun HanUniversity of Victoria-Genome British Columbia Proteomics Centre.
Natalie C MarshallMichael Smith Laboratories, University of British Columbia, Vancouver.
Sarah E WoodwardMichael Smith Laboratories, University of British Columbia, Vancouver.
Yanet ValdezMichael Smith Laboratories, University of British Columbia, Vancouver.
Christoph H BorchersDepartment of Biochemistry and Microbiology, University of Victoria, British Columbia.
Georgia Perona-WrightDepartment of Microbiology and Immunology, University of British Columbia, Vancouver.
B Brett FinlayMichael Smith Laboratories, University of British Columbia, Vancouver.

Funding

CIHR
6 · The paper itself

Abstract

Intestinal helminth infections occur predominantly in regions where exposure to enteric bacterial pathogens is also common. Helminth infections inhibit host immunity against microbial pathogens, which has largely been attributed to the induction of regulatory or type 2 (Th2) immune responses. Here we demonstrate an additional 3-way interaction in which helminth infection alters the metabolic environment of the host intestine to enhance bacterial pathogenicity. We show that an ongoing helminth infection increased colonization by Salmonella independently of T regulatory or Th2 cells. Instead, helminth infection altered the metabolic profile of the intestine, which directly enhanced bacterial expression of Salmonella pathogenicity island 1 (SPI-1) genes and increased intracellular invasion. These data reveal a novel mechanism by which a helminth-modified metabolome promotes susceptibility to bacterial coinfection.

Indexed as

MetabolomeAnimalsCoinfectionHeLa CellsHelminthiasisHumansIntestinal Diseases, ParasiticIntestinal MucosaIntestinesMiceMice, Inbred C57BLSalmonella InfectionsSalmonella typhimuriumTh2 Cellsbacterial infectionco-infectionhelminthsimmunomodulationintestinal metabolites.

Identifiers

PMID28368463
PMCPMC5853568

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.