Evidence map›Paper›PMID 31507587›Full record

ArticleFrontiers in immunology2019

ADAM17-Mediated Reduction in CD14

Kathryn Waller, Charlotte James, Anja de Jong, Laura Blackmore, Yun Ma, Andrew Stagg, David Kelsell, Michael O'Dwyer, Robert Hutchins, William Alazawi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Induction of dysfunctional CD14Frontiers in immunology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Circulating monocytes in acute pancreatitis.Frontiers in immunology · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Review
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

10 authors at 4 institutions in 2 countries.

Kathryn WallerBlizard Institute, Queen Mary University of London, London, United Kingdom.
Charlotte JamesBlizard Institute, Queen Mary University of London, London, United Kingdom.
Anja de JongBlizard Institute, Queen Mary University of London, London, United Kingdom.
Laura BlackmoreInstitute of Liver Studies and Transplantation, King's College London, London, United Kingdom.
Yun MaInstitute of Liver Studies and Transplantation, King's College London, London, United Kingdom.
Andrew StaggBlizard Institute, Queen Mary University of London, London, United Kingdom.
David KelsellBlizard Institute, Queen Mary University of London, London, United Kingdom.
Michael O'DwyerSt. Vincent's University Hospital, Dublin, Ireland.
Robert HutchinsHepatopancreaticobiliary Unit, Barts Health NHS Trust, London, United Kingdom.
William AlazawiBlizard Institute, Queen Mary University of London, London, United Kingdom.
Queen Mary University of London · GBKing's College London · GBBarts Health NHS Trust · GBSt. Vincent's University Hospital · IE

Funding

British Heart Foundation RG/13/19/30568Medical Research Council MR/L010402/1Medical Research Council MR/N00308X/1Wellcome Trust
6 · The paper itself

Abstract

Impaired immune responses and increased susceptibility to infection characterize acute inflammatory conditions such as pancreatitis and alcoholic hepatitis and are major causes of morbidity and mortality. However, the mechanisms that drive this apparent immune paresis remain poorly understood. Monocytes mediate host responses to damage and pathogens in health and disease, and three subsets of monocytes have been defined based on CD14 and CD16 expression. We sought to determine the changes in monocyte subsets in acute pancreatitis (AP) and acute alcoholic hepatitis (AAH), together with functional consequences and mechanisms that underlie this change. Peripheral blood mononuclear cells (PBMCs) from patients with AP or AAH were compared with healthy controls. Monocyte subsets were defined by HLA-DR, CD14, and CD16 expression. Changes in surface and intracellular protein expression and phosphorylation were determined by flow cytometry. Phenotype and function were assessed following stimulation with lipopolysaccharide (LPS) or other agonists in the presence of specific inhibitors of TNFα and a disintegrin and metalloproteinase 17 (ADAM17). Patients with AP and AAH had reduced CD14

Indexed as

ADAM17 ProteinBiomarkersCell SurvivalDisease SusceptibilityHepatitis, AlcoholicHumansImmunophenotypingLipopolysaccharide ReceptorsLipopolysaccharidesMonocytesPancreatitisReceptors, IgGADAM17 ProteinADAM17 protein, humanBiomarkersLipopolysaccharide ReceptorsLipopolysaccharidesReceptors, IgGacute alcoholic hepatitisacute pancreatitisADAM17infectioninflammationmonocytes

Identifiers

PMID31507587
PMCPMC6718469
OpenAlexW2964500472

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.