Evidence map›Paper›PMID 25372401›Full record

ArticlePloS one2014

Pharmacological inhibition of the chemokine CXCL16 diminishes liver macrophage infiltration and steatohepatitis in chronic hepatic injury.

Alexander Wehr, Christer Baeck, Florian Ulmer, Nikolaus Gassler, Kanishka Hittatiya, Tom Luedde, Ulf Peter Neumann, Christian Trautwein, Frank Tacke

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
4.3field-weighted citation impact, top 6% 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, 78 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Hepatic inflammatory responses in liver fibrosis.Nature reviews. Gastroenterology & hepatology · 2023
    Review
  5. Review
  6. Review
  7. The Role of Inflammation in Cholestatic Liver Injury.Journal of inflammation research · 2023
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. The Role of CXCL16 in the Pathogenesis of Cancer and Other Diseases.International journal of molecular sciences · 2021
    Review
  18. Protective effect of lyophilized sapodilla (Saudi journal of biological sciences · 2020
    Article
  19. Article
  20. 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

9 authors at 3 institutions in 1 country.

Alexander WehrDepartment of Medicine III, RWTH University-Hospital, Aachen, Germany.
Christer BaeckDepartment of Medicine III, RWTH University-Hospital, Aachen, Germany.
Florian UlmerDepartment of General, Visceral and Transplant Surgery, RWTH University-Hospital, Aachen, Germany.
Nikolaus GasslerInstitute of Pathology, RWTH University-Hospital, Aachen, Germany.
Kanishka HittatiyaDepartment of Pathology, Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Tom LueddeDepartment of Medicine III, RWTH University-Hospital, Aachen, Germany.
Ulf Peter NeumannDepartment of General, Visceral and Transplant Surgery, RWTH University-Hospital, Aachen, Germany.
Christian TrautweinDepartment of Medicine III, RWTH University-Hospital, Aachen, Germany.
Frank TackeDepartment of Medicine III, RWTH University-Hospital, Aachen, Germany.
RWTH Aachen University · DEUniversitätsklinikum Aachen · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a major cause of morbidity and mortality in developed countries, resulting in steatohepatitis (NASH), fibrosis and eventually cirrhosis. Modulating inflammatory mediators such as chemokines may represent a novel therapeutic strategy for NAFLD. We recently demonstrated that the chemokine receptor CXCR6 promotes hepatic NKT cell accumulation, thereby controlling inflammation in experimental NAFLD. In this study, we first investigated human biopsies (n = 20), confirming that accumulation of inflammatory cells such as macrophages is a hallmark of progressive NAFLD. Moreover, CXCR6 gene expression correlated with the inflammatory activity (ALT levels) in human NAFLD. We then tested the hypothesis that pharmacological inhibition of CXCL16 might hold therapeutic potential in NAFLD, using mouse models of acute carbon tetrachloride (CCl4)- and chronic methionine-choline-deficient (MCD) diet-induced hepatic injury. Neutralizing CXCL16 by i.p. injection of anti-CXCL16 antibody inhibited the early intrahepatic NKT cell accumulation upon acute toxic injury in vivo. Weekly therapeutic anti-CXCL16 administrations during the last 3 weeks of 6 weeks MCD diet significantly decreased the infiltration of inflammatory macrophages into the liver and intrahepatic levels of inflammatory cytokines like TNF or MCP-1. Importantly, anti-CXCL16 treatment significantly reduced fatty liver degeneration upon MCD diet, as assessed by hepatic triglyceride levels, histological steatosis scoring and quantification of lipid droplets. Moreover, injured hepatocytes up-regulated CXCL16 expression, indicating that scavenging functions of CXCL16 might be additionally involved in the pathogenesis of NAFLD. Targeting CXCL16 might therefore represent a promising novel therapeutic approach for liver inflammation and steatohepatitis.

Indexed as

Up-RegulationAnimalsCarbon Tetrachloride PoisoningChemokine CXCL16Chemokine CXCL6Chemokines, CXCChronic DiseaseFemaleHepatocytesHumansLiverMacrophagesMaleMiceNon-alcoholic Fatty Liver DiseaseReceptors, ScavengerChemokine CXCL16Chemokine CXCL6Chemokines, CXCCXCL16 protein, humanCxcl16 protein, mouseReceptors, Scavenger

Identifiers

PMID25372401
PMCPMC4221470
OpenAlexW2087983261

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.