Evidence map›Paper›PMID 29904132›Full record

ArticleClinical and translational gastroenterology2018

Decreased monocyte shedding of the migration inhibitor soluble CD18 in alcoholic hepatitis.

Sidsel Støy, Thomas Damgaard Sandahl, Anne Louise Hansen, Bent Deleuran, Thomas Vorup-Jensen, Hendrik Vilstrup, Tue Wenzel Kragstrup

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Clinical and translational gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Sidsel StøyDepartment of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark. sidsel.stoy@clin.au.dk.
Thomas Damgaard SandahlDepartment of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
Anne Louise HansenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Bent DeleuranDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Thomas Vorup-JensenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Hendrik VilstrupDepartment of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
Tue Wenzel KragstrupDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Aarhus University Hospital · DKAarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesDuring alcoholic hepatitis (AH) monocytes traverse the vascular boundaries and massively invade the liver. In principle, tissue extravasation can be limited through shedding of CD18 integrins from leukocytes, including monocytes. The soluble (s) product sCD18 conceals adhesion receptors on the endothelium, which reduces monocyte extravasation. In AH, monocytes are dysfunctional, but whether this involves their self-generated anti-migration is unknown. Our aim was, therefore, to investigate monocyte CD18 dynamics in AH.

methodsWe studied 50 AH patients and 20 healthy controls. We measured monocyte expression and conformational activation of CD18, plasma (P)-sCD18, stimulated in vitro CD18 shedding and P-sCD18 in a short-term chronic-binge mouse model.

resultsAH-derived monocytes had a 30-60% higher expression of active CD18 receptors (p < 0.01), but the sCD18 concentration per monocyte was reduced in vivo by 30% and in vitro by 120% (p < 0.01). Ethanol reduced the in vitro shedding of CD18 in the patients only. TNFα increased sCD18 concentration per monocyte, but less so in the patients (p < 0.04). P-sCD18 per monocyte was inversely related to disease severity. In early alcoholic liver disease, P-sCD18 was decreased in the mouse model.

conclusionsThe monocyte CD18 integrins are highly activated in AH and the single monocyte shedding of CD18 was decreased favoring tissue extravasation. Alcohol in itself and altered monocyte responsiveness to TNFα may explain this lowered shedding. TRANSLATIONAL IMPACT: The contribution of this mechanism to the excessive monocyte liver infiltration in AH should be further explored as it may serve as a potential therapeutic target to limit liver inflammation.

Indexed as

AnimalsCD18 AntigensCell MovementCells, CulturedEthanolFemaleHepatitis, AlcoholicHumansLeukocyte Migration-Inhibitory FactorsMacrophage ActivationMaleMiceMiddle AgedMonocytesPentoxifyllineTumor Necrosis Factor-alphaCD18 AntigensEthanolLeukocyte Migration-Inhibitory FactorsPentoxifyllineTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID29904132
PMCPMC6002386
OpenAlexW2808272196

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.