Evidence map›Paper›PMID 25121751›Full record

ArticleCell host & microbe2014

Epithelium-intrinsic NAIP/NLRC4 inflammasome drives infected enterocyte expulsion to restrict Salmonella replication in the intestinal mucosa.

Mikael E Sellin, Anna A Müller, Boas Felmy, Tamas Dolowschiak, Médéric Diard, Aubry Tardivel, Kendle M Maslowski, Wolf-Dietrich Hardt

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Cell host & microbe, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 254 papers.

0numbers the graph read from it
0cells of the map it votes in
254citing papers in PubMed
17.8field-weighted citation impact, top 1% 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

254 citing papers in PubMed, 402 citations in OpenAlex.

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  4. The Manipulation of Host Cells byInternational journal of molecular sciences · 2026
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  17. Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  18. Article
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  20. Infection strategies ofGut microbes reports · 2026
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Mikael E SellinInstitute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland. Electronic address: msellin@micro.biol.ethz.ch.
Anna A MüllerInstitute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
Boas FelmyInstitute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
Tamas DolowschiakInstitute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
Médéric DiardInstitute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
Aubry TardivelDepartment of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland.
Kendle M MaslowskiDepartment of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland; Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama 230-0045, Japan.
Wolf-Dietrich HardtInstitute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland. Electronic address: hardt@micro.biol.ethz.ch.
ETH Zurich · CHRIKEN Center for Integrative Medical Sciences · JPUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gut mucosal epithelium separates the host from the microbiota, but enteropathogens such as Salmonella Typhimurium (S.Tm) can invade and breach this barrier. Defenses against such acute insults remain incompletely understood. Using a murine model of Salmonella enterocolitis, we analyzed mechanisms limiting pathogen loads in the epithelium during early infection. Although the epithelium-invading S.Tm replicate initially, this intraepithelial replicative niche is restricted by expulsion of infected enterocytes into the lumen. This mechanism is compromised if inflammasome components (NAIP1-6, NLRC4, caspase-1/-11) are deleted, or ablated specifically in the epithelium, resulting in ∼100-fold higher intraepithelial loads and accelerated lymph node colonization. Interestingly, the cytokines downstream of inflammasome activation, interleukin (IL)-1α/β and IL-18, appear dispensable for epithelial restriction of early infection. These data establish the role of an epithelium-intrinsic inflammasome, which drives expulsion of infected cells to restrict the pathogen's intraepithelial proliferation. This may represent a general defense mechanism against mucosal infections.

Indexed as

AnimalsApoptosis Regulatory ProteinsCalcium-Binding ProteinsCecumEnterocytesHost-Pathogen InteractionsInflammasomesIntestinal MucosaMice, Inbred C57BLMice, KnockoutNeuronal Apoptosis-Inhibitory ProteinSalmonella InfectionsSalmonella typhimuriumApoptosis Regulatory ProteinsCalcium-Binding ProteinsInflammasomesIpaf protein, mouseNaip1 protein, mouseNeuronal Apoptosis-Inhibitory Protein

Identifiers

PMID25121751
OpenAlexW2106145925

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.