Evidence map›Paper›PMID 27366100›Full record

ArticleJournal of inflammation research2016

TNF-related apoptosis-inducing ligand deficiency enhances survival in murine colon ascendens stent peritonitis.

Katharina Beyer, Laura Stollhof, Christian Poetschke, Wolfram von Bernstorff, Lars Ivo Partecke, Stephan Diedrich, Stefan Maier, Barbara M Bröker, Claus-Dieter Heidecke

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Katharina BeyerDepartment of General, Visceral, Thoracic, and Vascular Surgery, University of Greifswald, Greifswald, Germany.
Laura StollhofDepartment of General, Visceral, Thoracic, and Vascular Surgery, University of Greifswald, Greifswald, Germany.
Christian PoetschkeInstitute of Immunology, University of Greifswald, Greifswald, Germany.
Wolfram von BernstorffDepartment of General, Visceral, Thoracic, and Vascular Surgery, University of Greifswald, Greifswald, Germany.
Lars Ivo ParteckeDepartment of General, Visceral, Thoracic, and Vascular Surgery, University of Greifswald, Greifswald, Germany.
Stephan DiedrichDepartment of General, Visceral, Thoracic, and Vascular Surgery, University of Greifswald, Greifswald, Germany.
Stefan MaierDepartment of General, Visceral, Thoracic, and Vascular Surgery, University of Greifswald, Greifswald, Germany.
Barbara M BrökerInstitute of Immunology, University of Greifswald, Greifswald, Germany.
Claus-Dieter HeideckeDepartment of General, Visceral, Thoracic, and Vascular Surgery, University of Greifswald, Greifswald, Germany.
Universitätsmedizin Greifswald · DEUniversität Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApart from inducing apoptosis in tumor cells, tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) influences inflammatory reactions. Murine colon ascendens stent peritonitis (CASP) represents a model of diffuse peritonitis. Recently, it has been demonstrated that administration of exogenous TRAIL not only induces apoptosis in neutrophils but also enhances survival in this model. The aim of this study was to examine the impact of genetic TRAIL deficiency on the course of CASP.

methodsPeritonitis was induced in 6- to 8-week-old female TRAIL (-/-) mice as well as in wild-type mice. The sepsis severity score and survival of mice were monitored. Bacterial loads in blood as well as in the lymphoid organs were examined. Additionally, the number of apoptotic cells within the lymphoid organs was determined.

resultsAs early as 8 hours postinduction of CASP, TRAIL (-/-) mice were significantly more affected by sepsis than wild-type mice, as measured by the sepsis severity score. However, during the further course of sepsis, TRAIL deficiency led to significantly decreased sepsis severity scores, resulting in an enhanced overall survival in TRAIL (-/-) mice. The better survival of TRAIL (-/-) mice was accompanied by a decreased bacterial load within the blood. In marked contrast, the number of apoptotic cells within the lymphoid organs was highly increased in TRAIL (-/-) mice 20 hours after induction of CASP.

conclusionHence, exogenous and endogenous TRAIL is protective during the early phase of sepsis, while endogenous TRAIL appears to be detrimental in the later course of this disease.

Indexed as

CASPinflammationmicesepsisTRAIL

Identifiers

PMID27366100
PMCPMC4914030
OpenAlexW2431214249

What OpenQuestion holds

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Registered trials

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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.