Evidence map›Paper›PMID 31072958›Full record

ArticleDisease models & mechanisms2019

Glucocorticoids inhibit macrophage differentiation towards a pro-inflammatory phenotype upon wounding without affecting their migration.

Yufei Xie, Sofie Tolmeijer, Jelle M Oskam, Tijs Tonkens, Annemarie H Meijer, Marcel J M Schaaf

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Disease models & mechanisms, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
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  16. Melanocyte-dependent macrophage redistribution enhances skin immunity upon acute stress.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Article
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  19. Molecular dynamics of inflammation resolution: therapeutic implications.Frontiers in cell and developmental biology · 2025
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  20. Article

7 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Yufei XieAnimal Science and Health Cluster, Institute of Biology, Leiden University, 2333CC Leiden, The Netherlands.ORCID 0000-0001-6668-3420
Sofie TolmeijerAnimal Science and Health Cluster, Institute of Biology, Leiden University, 2333CC Leiden, The Netherlands.
Jelle M OskamAnimal Science and Health Cluster, Institute of Biology, Leiden University, 2333CC Leiden, The Netherlands.
Tijs TonkensAnimal Science and Health Cluster, Institute of Biology, Leiden University, 2333CC Leiden, The Netherlands.
Annemarie H MeijerAnimal Science and Health Cluster, Institute of Biology, Leiden University, 2333CC Leiden, The Netherlands.ORCID 0000-0002-1325-0725
Marcel J M SchaafAnimal Science and Health Cluster, Institute of Biology, Leiden University, 2333CC Leiden, The Netherlands m.j.m.schaaf@biology.leidenuniv.nl.ORCID 0000-0002-5859-8936
Leiden University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoid drugs are widely used to treat immune-related diseases, but their use is limited by side effects and by resistance, which especially occurs in macrophage-dominated diseases. In order to improve glucocorticoid therapies, more research is required into the mechanisms of glucocorticoid action. In the present study, we have used a zebrafish model for inflammation to study glucocorticoid effects on the innate immune response. In zebrafish larvae, the migration of neutrophils towards a site of injury is inhibited upon glucocorticoid treatment, whereas migration of macrophages is glucocorticoid resistant. We show that wounding-induced increases in the expression of genes that encode neutrophil-specific chemoattractants (Il8 and Cxcl18b) are attenuated by the synthetic glucocorticoid beclomethasone, but that beclomethasone does not attenuate the induction of the genes encoding Ccl2 and Cxcl11aa, which are required for macrophage recruitment. RNA sequencing on FACS-sorted macrophages shows that the vast majority of the wounding-induced transcriptional changes in these cells are inhibited by beclomethasone, whereas only a small subset is glucocorticoid-insensitive. As a result, beclomethasone decreases the number of macrophages that differentiate towards a pro-inflammatory (M1) phenotype, which we demonstrated using a

Indexed as

Amputation, SurgicalAnimalsBeclomethasoneCell DifferentiationCell MovementCell TrackingChemotactic FactorsGene Expression RegulationGlucocorticoidsInflammationLarvaMacrophagesMorpholinosNeutrophilsPhenotypeTranscriptomeBeclomethasoneChemotactic FactorsGlucocorticoidsMorpholinosGlucocorticoidsInflammationLeukocyte migrationMacrophage differentiationTail amputationZebrafish

Identifiers

PMID31072958
PMCPMC6550045
OpenAlexW2952679984

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.