Evidence map›Paper›PMID 24253103›Full record

ArticleMucosal immunology2014

Gal-lectin-dependent contact activates the inflammasome by invasive Entamoeba histolytica.

L Mortimer, F Moreau, S Cornick, K Chadee

Abstract read
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In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Immunomodulatory effect of extracellular vesicles fromFrontiers in cellular and infection microbiology · 2022
    Article
  8. Gasdermins in Innate Host Defense AgainstFrontiers in immunology · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. The NF-κB Pathway: Modulation byFrontiers in cellular and infection microbiology · 2021
    Review
  13. Article
  14. Frontiers in microbiology · 2020
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. How Inflammasomes Inform Adaptive Immunity.Journal of molecular biology · 2018
    Review
  20. mBio · 2017
    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

4 authors.

L MortimerFaculty of Medicine, Department of Microbiology, Immunology and Infectious Diseases, Snyder Institute for Chronic Diseases, Gastrointestinal Research Group, University of Calgary, Calgary, Alberta, Canada.
F MoreauFaculty of Medicine, Department of Microbiology, Immunology and Infectious Diseases, Snyder Institute for Chronic Diseases, Gastrointestinal Research Group, University of Calgary, Calgary, Alberta, Canada.
S CornickFaculty of Medicine, Department of Microbiology, Immunology and Infectious Diseases, Snyder Institute for Chronic Diseases, Gastrointestinal Research Group, University of Calgary, Calgary, Alberta, Canada.
K ChadeeFaculty of Medicine, Department of Microbiology, Immunology and Infectious Diseases, Snyder Institute for Chronic Diseases, Gastrointestinal Research Group, University of Calgary, Calgary, Alberta, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Entamoeba histolytica (Eh) is an extracellular protozoan parasite of the human colon, which occasionally breaches the intestinal barrier. Eradicating ameba that invades is essential for host survival. A defining but uncharacterized feature of amebic invasion is direct contact between ameba and host cells. This event corresponds with a massive pro-inflammatory response. To date, pathogen recognition receptors (PRRs) that are activated by contact with viable Eh are unknown. Here we show that the innate immune system responds in a qualitatively different way to contact with viable Eh vs. soluble ligands produced by viable or dead ameba. This unique Eh Gal-lectin contact-dependent response in macrophages was mediated by activation of the inflammasome. Soluble native Gal-lectin did not induce inflammasome activation, but was sufficient for transcriptional priming of the inflammasome and non-inflammasome-dependent pro-inflammatory cytokine release. We conclude the inflammasome is a pathogenicity sensor for invasive Eh and identify for the first time a PRR that specifically responds to contact with intact parasites in a manner that accords with scale immune response to parasite invasion.

Indexed as

InflammasomesAnimalsAntigens, ProtozoanCaspase 1Entamoeba histolyticaEntamoebiasisEpitopesGerbillinaeMacrophagesMaleMembrane GlycoproteinsProtein BindingProtozoan ProteinsAntigens, ProtozoanCaspase 1EpitopesInflammasomesMembrane GlycoproteinsProtozoan Proteins

Identifiers

PMID24253103

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.