Evidence map›Paper›PMID 34497340›Full record

ArticleMucosal immunology2022

STAT1 coordinates intestinal epithelial cell death during gastrointestinal infection upstream of Caspase-8.

Iris Stolzer, Laura Schickedanz, Mircea T Chiriac, Rocío López-Posadas, Guntram A Grassl, Jochen Mattner, Stefan Wirtz, Beate Winner, Markus F Neurath, Claudia Günther

Open access · hybridAbstract read
In one paragraph

Article in Mucosal immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.8field-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

15 citing papers in PubMed, 25 citations in OpenAlex.

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  15. Cross-Talk Between the Intestinal Epithelium andFrontiers in microbiology · 2022
    Review
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

10 authors at 2 institutions in 1 country.

Iris StolzerDepartment of Medicine 1, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität (FAU), Erlangen, Germany.
Laura SchickedanzDepartment of Medicine 1, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität (FAU), Erlangen, Germany.
Mircea T ChiriacDepartment of Medicine 1, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität (FAU), Erlangen, Germany.
Rocío López-PosadasDepartment of Medicine 1, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität (FAU), Erlangen, Germany.
Guntram A GrasslInstitute of Medical Microbiology and Hospital Epidemiology, Hannover Medical School and German Center for Infection Research (DZIF), Hannover, Germany.
Jochen MattnerMikrobiologisches Institut-Klinische Mikrobiologie, Immunologie und Hygiene, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität (FAU), Erlangen, Germany.
Stefan WirtzDepartment of Medicine 1, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität (FAU), Erlangen, Germany.
Beate WinnerDepartment of Stem Cell Biology, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität (FAU), Erlangen, Germany.
Markus F NeurathDepartment of Medicine 1, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität (FAU), Erlangen, Germany.
Claudia GüntherDepartment of Medicine 1, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität (FAU), Erlangen, Germany. c.guenther@uk-erlangen.de.
Universitätsklinikum Erlangen · DEGerman Center for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal homeostasis and the maintenance of the intestinal epithelial barrier are essential components of host defense during gastrointestinal Salmonella Typhimurium infection. Both require a strict regulation of cell death. However, the molecular pathways regulating epithelial cell death have not been completely understood. Here, we elucidated the contribution of central mechanisms of regulated cell death and upstream regulatory components during gastrointestinal infection. Mice lacking Caspase-8 in the intestinal epithelium are highly sensitive towards bacterial induced enteritis and intestinal inflammation, resulting in an enhanced lethality of these mice. This phenotype was associated with an increased STAT1 activation during Salmonella infection. Cell death, barrier breakdown and systemic infection were abrogated by an additional deletion of STAT1 in Casp8

Indexed as

AnimalsCaspase 8Cell DeathEpithelial CellsGastrointestinal DiseasesHomeostasisMiceMice, Inbred C57BLMice, KnockoutSalmonella InfectionsSalmonella typhimuriumSignal TransductionSTAT1 Transcription FactorCaspase 8STAT1 Transcription Factor

Identifiers

PMID34497340
PMCPMC8732278
OpenAlexW3196395125

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.