Evidence map›Paper›PMID 23216784›Full record

ArticleExperimental & translational stroke medicine2012

Indoleamine-2,3-dioxygenase activity in experimental human endotoxemia.

Jan-Sören Padberg, Matijs Van Meurs, Jan T Kielstein, Jens Martens-Lobenhoffer, Stefanie M Bode-Böger, Jan G Zijlstra, Csaba P Kovesdy, Philipp Kümpers

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental & translational stroke medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 49% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
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

8 authors at 5 institutions in 3 countries.

Jan-Sören Padberg *Department of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Campus A1, Münster 48149, Germany.
Matijs Van Meurs *Department of Critical Care, University Medical Center Groningen, Hanzeplein 1, University of Groningen, Groningen, GZ, 9713, The Netherlands.
Jan T KielsteinDepartment of Nephrology & Hypertension, Hannover Medical School, Carl-Neuberg-Strasse 1, Hannover, 30625, Germany.
Jens Martens-LobenhofferInstitute for Clinical Pharmacology, Otto-von-Guericke University Magdeburg, Leipziger Straße 44, Magdeburg, 39120, Germany.
Stefanie M Bode-BögerInstitute for Clinical Pharmacology, Otto-von-Guericke University Magdeburg, Leipziger Straße 44, Magdeburg, 39120, Germany.
Jan G ZijlstraDepartment of Critical Care, University Medical Center Groningen, Hanzeplein 1, University of Groningen, Groningen, GZ, 9713, The Netherlands.
Csaba P KovesdyDivisions of Nephrology, University of Virginia, Charlottesville, Virginia & Salem VA Medical Center 1970 Roanoke Blvd, Salem, VA, 24153, USA.
Philipp KümpersDepartment of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Campus A1, Münster 48149, Germany.
Otto-von-Guericke University Magdeburg · DEUniversity Hospital Münster · DEUniversity of Groningen · NLMedizinische Hochschule Hannover · DESalem VA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelled

backgroundExcessive tryptophan metabolism to kynurenine by the rate-limiting enzyme endothelial indoleamine 2,3-dioxygenase 1 (IDO) controls arterial vessel relaxation and causes hypotension in murine endotoxemia. However, its relevance in human endotoxemia has not been investigated so far. We thus aimed to study changes in blood pressure in parallel with tryptophan and kynurenine levels during experimental endotoxemia in humans.

findingsSix healthy male volunteers were given E. coli lipopolysaccharide (LPS; 4 ng/kg) as a 1-min intravenous infusion. They had levels of soluble E-Selectin and soluble vascular cell adhesion molecule-1 as well as IDO activity assessed as the kynurenine-to-tryptophan plasma ratio by liquid chromatography-tandem mass spectrometry at various time points during a 24 h time course. During endotoxemia, IDO activity significantly increased, reaching peak levels at 8 h after LPS infusion (44.0 ± 15.2 vs. 29.4 ± 6.8 at baseline, P<0.0001). IDO activity correlated inversely with the development of hypotension as shown by random effects linear regression models. Finally, IDO activity exhibited a kinetic profile similar to that of soluble endothelial-specific adhesion molecules.

conclusionsLPS is a triggering factor for the induction of IDO in men. Our findings strongly support the concept that the induction of IDO in the vascular endothelium contributes to hypotension in human sepsis.

Identifiers

PMID23216784
PMCPMC3560239
OpenAlexW2159696587

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.