Evidence map›Paper›PMID 38471395›Full record

ArticleEBioMedicine2024

Tryptophan degradation as a systems phenomenon in inflammation - an analysis across 13 chronic inflammatory diseases.

Danielle M M Harris, Silke Szymczak, Sven Schuchardt, Johannes Labrenz, Florian Tran, Lina Welz, Hanna Graßhoff, Henner Zirpel, Melike Sümbül, Mhmd Oumari and 12 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

37 citing papers in PubMed, 39 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

22 authors at 6 institutions in 1 country.

Danielle M M HarrisInstitute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany; Institute for Human Nutrition and Food Science, Division Nutriinformatics, Kiel University, Kiel, Germany.
Silke SzymczakInstitute of Medical Biometry and Statistics, University of Lübeck, University Medical Center Schleswig-Holstein, Campus Lübeck, Lübeck, Germany.
Sven SchuchardtFraunhofer Institute for Toxicology and Experimental Medicine (ITEM), Hanover, Germany.
Johannes LabrenzInstitute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Florian TranInstitute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany; Department of Internal Medicine I, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Lina WelzInstitute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany; Institute for Human Nutrition and Food Science, Division Nutriinformatics, Kiel University, Kiel, Germany.
Hanna GraßhoffDepartment of Rheumatology University Medical Center Schleswig-Holstein, Campus Lübeck, Lübeck, Germany.
Henner ZirpelComprehensive Center for Inflammation Medicine, University Medical Center Schleswig-Holstein, Lübeck, Germany.
Melike SümbülDepartment of Dermatology, University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Mhmd OumariInstitute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Nils EngelbogenInstitute of Clinical Chemistry, University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Ralf JunkerInstitute of Clinical Chemistry, University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Claudio ConradDepartment of Internal Medicine I, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Diamant ThaçiComprehensive Center for Inflammation Medicine, University Medical Center Schleswig-Holstein, Lübeck, Germany.
Norbert FreyDepartment of Medicine III: Cardiology, Angiology, and Pneumology, Heidelberg University, Heidelberg, Germany.
Andre FrankeInstitute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Stephan WeidingerDepartment of Dermatology, University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Bimba HoyerDepartment of Internal Medicine I, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Philip RosenstielInstitute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Silvio WaschinaInstitute for Human Nutrition and Food Science, Division Nutriinformatics, Kiel University, Kiel, Germany.
Stefan SchreiberInstitute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany; Department of Internal Medicine I, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Konrad AdenInstitute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany; Department of Internal Medicine I, Kiel University and University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany. Electronic address: k.aden@ikmb.uni-kiel.de.
Christian-Albrechts-Universität zu Kiel · DEHochschule für Angewandte Wissenschaften Kiel · DEUniversity of Lübeck · DEClinical Research Center Kiel · DEFraunhofer Institute for Toxicology and Experimental Medicine · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic inflammatory diseases (CIDs) are systems disorders that affect diverse organs including the intestine, joints and skin. The essential amino acid tryptophan (Trp) can be broken down to various bioactive derivatives important for immune regulation. Increased Trp catabolism has been observed in some CIDs, so we aimed to characterise the specificity and extent of Trp degradation as a systems phenomenon across CIDs.

methodsWe used high performance liquid chromatography and targeted mass spectrometry to assess the serum and stool levels of Trp and Trp derivatives. Our retrospective study incorporates both cross-sectional and longitudinal components, as we have included a healthy population as a reference and there are also multiple observations per patient over time.

findingsWe found reduced serum Trp levels across the majority of CIDs, and a prevailing negative relationship between Trp and systemic inflammatory marker C-reactive protein (CRP). Notably, serum Trp was low in several CIDs even in the absence of measurable systemic inflammation. Increases in the kynurenine-to-Trp ratio (Kyn:Trp) suggest that these changes result from increased degradation along the kynurenine pathway.

interpretationIncreases in Kyn:Trp indicate the kynurenine pathway as a major route for CID-related Trp metabolism disruption and the specificity of the network changes indicates excessive Trp degradation relative to other proteogenic amino acids. Our results suggest that increased Trp catabolism is a common metabolic occurrence in CIDs that may directly affect systemic immunity.

fundingThis work was supported by the DFG Cluster of Excellence 2167 "Precision medicine in chronic inflammation" (KA, SSchr, PR, BH, SWa), the BMBF (e:Med Juniorverbund "Try-IBD" 01ZX1915A and 01ZX2215, the e:Med Network iTREAT 01ZX2202A, and GUIDE-IBD 031L0188A), EKFS (2020_EKCS.11, KA), DFG RU5042 (PR, KA), and Innovative Medicines Initiative 2 Joint Undertakings ("Taxonomy, Treatments, Targets and Remission", 831434, "ImmUniverse", 853995, "BIOMAP", 821511).

Indexed as

Inflammatory Bowel DiseasesTryptophanChronic DiseaseCross-Sectional StudiesHumansInflammationKynurenineRetrospective StudiesKynurenineTryptophanInflammationKynurenine pathwayMetabolismMetabolitesMetabolomicsTryptophan

Identifiers

PMID38471395
PMCPMC10943670
OpenAlexW4392672294

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.