Evidence map›Paper›PMID 24280937›Full record

ArticleMucosal immunology2014

Nlrp3 activation in the intestinal epithelium protects against a mucosal pathogen.

George X Song-Zhao, Naren Srinivasan, Johanna Pott, Dilair Baban, Gad Frankel, Kevin J Maloy

Open access · bronzeAbstract read
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 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. GSDMD deficiency mitigates intestinal damage via macrophage pyroptosis control in experimental NEC.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  8. Review
  9. Link Between Oral and Gut Microbiomes: The Oral-Gut Axis.Advances in experimental medicine and biology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Article
  19. Review
  20. Review

24 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

George X Song-Zhao *Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK.
Naren Srinivasan *Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK.
Johanna PottSir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK.
Dilair BabanWellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Gad FrankelMRC Centre for Molecular Bacteriology and Infection, Division of Cell and Molecular Biology, Imperial College London, London, UK.
Kevin J MaloySir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK.
University of Oxford · GBCentre for Human Genetics · GBMRC Laboratory for Molecular Cell Biology · GB

Funding

Medical Research Council MR/J006874/1Medical Research Council MR/K011898/1Wellcome Trust 086354Wellcome Trust 091911
6 · The paper itself

Abstract

Polymorphisms in the intracellular pattern recognition receptor gene NLRP3 (NLR family, pyrin domain containing 3) have been associated with susceptibility to Crohn's disease, a type of inflammatory bowel disease. Following tissue damage or infection, NLRP3 triggers the formation of inflammasomes, containing NLRP3, ASC (apoptosis-associated speck-like protein containing a CARD domain), and caspase-1, that mediate secretion of interleukin (IL)-1β and IL-18. However, the precise role of NLRP3 inflammasomes in mucosal inflammation and barrier protection remains unclear. Here we show that upon infection with the attaching/effacing intestinal pathogen Citrobacter rodentium, Nlrp3(-/-) and Asc(-/-) mice displayed increased bacterial colonization and dispersion, more severe weight loss, and exacerbated intestinal inflammation. Analyses of irradiation bone marrow chimeras revealed that protection from disease was mediated through Nlrp3 activation in nonhematopoietic cells and was initiated very early after infection. Thus, early activation of Nlrp3 in intestinal epithelial cells limits pathogen colonization and prevents subsequent pathology, potentially providing a functional link between NLRP3 polymorphisms and susceptibility to inflammatory bowel disease.

Indexed as

Transcriptional ActivationAnimalsApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Citrobacter rodentiumDisease Models, AnimalDisease ResistanceEnterobacteriaceae InfectionsHost-Pathogen InteractionsInflammationIntestinal MucosaMiceMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1NLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePycard protein, mouse

Identifiers

PMID24280937
PMCPMC4048180
OpenAlexW2094123482

What OpenQuestion holds

Textmetadata
LicenceTDM
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.