Evidence map›Paper›PMID 31666808›Full record

ArticleTherapeutic advances in gastroenterology2019

Increased expression of kynurenine aminotransferases mRNA in lymphocytes of patients with inflammatory bowel disease.

Ewa Dudzińska, Kinga Szymona, Renata Kloc, Paulina Gil-Kulik, Tomasz Kocki, Małgorzata Świstowska, Jacek Bogucki, Janusz Kocki, Ewa M Urbanska

Open access · goldAbstract read
In one paragraph

Article in Therapeutic advances in gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

26 citing papers in PubMed, 42 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 1 institution in 1 country.

Ewa DudzińskaMedical University of Lublin, Chodźki 1 Street, Lublin, 20-093, Lubelskie, Poland.ORCID https://orcid.org/0000-0003-3077-4288
Kinga SzymonaMedical University of Lublin, Lublin, Lubelskie, Poland.
Renata KlocDepartment of Experimental and Clinical Pharmacology, Medical University of Lublin, Lublin, Lubelskie, Poland.
Paulina Gil-KulikDepartment of Clinical Genetics, Medical University of Lublin, Lublin, Lubelskie, Poland.
Tomasz KockiDepartment of Experimental and Clinical Pharmacology, Medical University of Lublin, Lublin, Lubelskie, Poland.
Małgorzata ŚwistowskaDepartment of Clinical Genetics, Medical University of Lublin, Lublin, Lubelskie, Poland.
Jacek BoguckiDepartment of Clinical Genetics, Medical University of Lublin, Lublin, Lubelskie, Poland.
Janusz KockiDepartment of Clinical Genetics, Medical University of Lublin, Lublin, Lubelskie, Poland.
Ewa M UrbanskaDepartment of Experimental and Clinical Pharmacology, Medical University of Lublin, Lublin, Lubelskie, Poland.
Medical University of Lublin · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundComplex interaction of genetic defects with environmental factors seems to play a substantial role in the pathogenesis of inflammatory bowel disease (IBD). Accumulating data implicate a potential role of disturbed tryptophan metabolism in IBD. Kynurenic acid (KYNA), a derivative of tryptophan (TRP) along the kynurenine (KYN) pathway, displays cytoprotective and immunomodulating properties, whereas 3-OH-KYN is a cytotoxic compound, generating free radicals.

methodsThe expression of lymphocytic mRNA encoding enzymes synthesizing KYNA (KAT I-III) and serum levels of TRP and its metabolites were evaluated in 55 patients with IBD, during remission or relapse [27 patients with ulcerative colitis (UC) and 28 patients with Crohn's disease (CD)] and in 50 control individuals.

resultsThe increased expression of KAT1 and KAT3 mRNA characterized the entire cohorts of patients with UC and CD, as well as relapse-remission subsets. Expression of KAT2 mRNA was enhanced in patients with UC and in patients with CD in remission. In the entire cohorts of UC or CD, TRP levels were lower, whereas KYN, KYNA and 3-OH-KYN were not altered. When analysed in subsets of patients with UC and CD (active phase-remission), KYNA level was significantly lower during remission than relapse, yet not

conclusionThe presented data indicate that IBD is associated with an enhanced expression of genes encoding KYNA biosynthetic enzymes in lymphocytes; however, additional mechanisms appear to influence KYNA levels. Higher metabolic conversion of serum TRP in IBD seems to be followed by the functional shift of KYN pathway towards the arm producing KYNA during exacerbation. We propose that KYNA, possibly

Indexed as

Crohn’s diseaseHPLCkynurenine pathwayPCRulcerative colitis

Identifiers

PMID31666808
PMCPMC6801885
OpenAlexW2980348501

What OpenQuestion holds

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LicenceCC BY-NC
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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.