Evidence map›Paper›PMID 26133108›Full record

ArticleClinical and translational gastroenterology2015

Increased Serum Levels of LIGHT/TNFSF14 in Nonalcoholic Fatty Liver Disease: Possible Role in Hepatic Inflammation.

Kari Otterdal, John Willy Haukeland, Arne Yndestad, Tuva B Dahl, Sverre Holm, Filip M Segers, Ivar P Gladhaug, Zbigniew Konopski, Jan Kristian Damås, Bente Halvorsen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  6. LIGHT Amplification by NF-Mediators of inflammation · 2023
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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

11 authors at 3 institutions in 1 country.

Kari Otterdal1] Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway [2] Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
John Willy HaukelandDepartment of Gastroenterology, Oslo University Hospital Ullevål, Oslo, Norway.
Arne Yndestad1] Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway [2] Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway [3] K.G. Jebsen Inflammatory Research Center, Oslo, Norway.
Tuva B Dahl1] Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway [2] Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Sverre HolmResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Filip M SegersResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Ivar P Gladhaug1] Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway [2] Department of Hepato-Pancreato-Biliary Surgery, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Zbigniew KonopskiDepartment of Gastroenterology, Oslo University Hospital Ullevål, Oslo, Norway.
Jan Kristian Damås1] Centre of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, St Olavs Hospital, Trondheim, Norway [2] Department of Infectious Diseases, St Olavs Hospital, Trondheim, Norway.
Bente Halvorsen1] Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway [2] Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway [3] K.G. Jebsen Inflammatory Research Center, Oslo, Norway.
Pål Aukrust1] Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway [2] Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway [3] K.G. Jebsen Inflammatory Research Center, Oslo, Norway [4] Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Oslo University Hospital · NOUniversity of Oslo · NONorwegian University of Science and Technology · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe tumor necrosis factor superfamily member 14, LIGHT (homologous to lymphotoxin, exhibits inducible expression, and competes with HSV glycoprotein D for herpes virus entry mediator (HVEM), a receptor expressed by T lymphocytes), has been involved in various autoimmune disorders and has been shown to influence hepatic lipid metabolism. We hypothesized that LIGHT could also have a pathogenic role in nonalcoholic fatty liver disease (NAFLD).

methodsSerum levels of LIGHT in NAFLD patients and control subjects, as well as LIGHT and interleukin (IL)-8 released from Huh7 (human hepatoma cell line) hepatocytes, were determined by enzyme-linked immunosorbent assay. The mRNA expression of LIGHT in the liver tissue and mRNA levels of LIGHT and IL-8 in Huh7 hepatocytes were assessed by real-time quantitative reverse transcription-PCR.

results(i) Serum levels of LIGHT were significantly elevated in NAFLD patients (n=66) as compared with healthy controls (n=16), with no differences between simple steatosis (n=34) and nonalcoholic steatohepatitis (NASH) (n=32). (ii) Within the liver, NAFLD patients (n=14) had significantly increased mRNA levels of the two LIGHT receptors, herpes virus entry mediator and lymphotoxin β receptor (LTβR), as compared with controls (n=7), with no difference between simple steatosis (n=8) and NASH (n=6). (iii) LIGHT markedly increased the release of IL-8 in Huh7 hepatocytes in a time- and dose-dependent manner. (iv) The reactive oxygen species (ROS) H2O2 (hydrogen peroxide) enhanced the LIGHT-mediated release of IL-8 in Huh7 hepatocytes.

conclusionWe show increased levels of LIGHT and its two membrane-bound receptors in NAFLD, potentially promoting hepatic inflammation through ROS interaction. Our findings should encourage further studies on the role of LIGHT in NAFLD development and progression.

Identifiers

PMID26133108
PMCPMC4816254
OpenAlexW1527359472

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.