Evidence map›Paper›PMID 24280936›Full record

ArticleMucosal immunology2014

NLRC4 expression in intestinal epithelial cells mediates protection against an enteric pathogen.

S Nordlander, J Pott, K 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 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Pooled it
  2. Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. NLRC4, inflammation and colorectal cancer (Review).International journal of oncology · 2024
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Inflammasome-Independent Roles of NLR and ALR Family Members.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  14. Canonical Inflammasomes.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  15. Review
  16. Article
  17. The autoinflammation-associated NLRC4Frontiers in immunology · 2023
    Article
  18. Article
  19. Epithelial Pyroptosis in Host Defense.Journal of molecular biology · 2022
    Review
  20. Review

27 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

3 authors at 1 institution in 1 country.

S NordlanderSir William Dunn School of Pathology, University of Oxford, Oxford, UK.
J PottSir William Dunn School of Pathology, University of Oxford, Oxford, UK.
K J MaloySir William Dunn School of Pathology, University of Oxford, Oxford, UK.
University of Oxford · GB

Funding

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

Abstract

The inflammasomes have an important role in connecting the detection of endogenous and microbial danger signals to caspase-1 activation and induction of protective immune responses. NLRC4 is a cytosolic NOD (nucleotide binding and oligomerization domain)-like receptor (NLR) that can trigger inflammasome formation in response to bacterial flagellin, an immunodominant antigen in the intestine. To characterize the role of NLRC4 in bacterially triggered intestinal inflammation, we used the murine pathogen Citrobacter rodentium, an extracellular, attaching/effacing bacterium similar to enterohemorrhagic Escherichia coli and enteropathogenic E. coli. Following infection with C. rodentium, we found that Nlrc4(-/-) mice developed more severe weight loss, increased bacterial colonization levels, and exacerbated intestinal inflammation compared with wild-type counterparts. Nlrc4(-/-) mice mounted robust adaptive immune responses but were unable to control early colonization by C. rodentium, suggesting that a defect in innate immunity was responsible. Experiments using bone marrow (BM) chimeras revealed that the protective effects of NLRC4 were dependent on its expression in non-hematopoietic cells, and quantitative PCR (Q-PCR) analyses revealed that NLRC4 was highly expressed in epithelial crypts but not in intestinal stroma. Thus, early NLRC4 sensing in intestinal epithelial cells regulates colonization by an extracellular bacterial pathogen and limits subsequent intestinal damage.

Indexed as

Gene ExpressionAdaptive ImmunityAnimalsApoptosis Regulatory ProteinsCalcium-Binding ProteinsCitrobacter rodentiumDisease Models, AnimalEnterobacteriaceae InfectionsEpithelial CellsEscherichia coliHost-Pathogen InteractionsInflammationInterleukin-18Intestinal MucosaMiceMice, KnockoutApoptosis Regulatory ProteinsCalcium-Binding ProteinsInterleukin-18Ipaf protein, mouse

Identifiers

PMID24280936
PMCPMC4020766
OpenAlexW2033093833

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.