Evidence map›Paper›PMID 34560894›Full record

ArticleArthritis research & therapy2021

Monocyte transcriptomes from patients with axial spondyloarthritis reveal dysregulated monocytopoiesis and a distinct inflammatory imprint.

Fabian Karow, Biljana Smiljanovic, Joachim R Grün, Denis Poddubnyy, Fabian Proft, Alice Talpin, Christophe Hue, Anne Boland, Jean-François Deleuze, Henri-Jean Garchon and 8 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

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  6. The bone marrow side of axial spondyloarthritis.Nature reviews. Rheumatology · 2023
    Review
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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

18 authors at 5 institutions in 4 countries.

Fabian KarowMedizinische Klinik für Gastroenterologie, Infektiologie und Rheumatologie, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
Biljana SmiljanovicMedizinische Klinik für Rheumatologie und Klinische Immunologie, Campus Mitte, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Joachim R GrünDeutsches Rheumaforschungszentrum (DRFZ), A Leibniz Institute, Berlin, Germany.
Denis PoddubnyyMedizinische Klinik für Gastroenterologie, Infektiologie und Rheumatologie, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
Fabian ProftMedizinische Klinik für Gastroenterologie, Infektiologie und Rheumatologie, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
Alice TalpinInfection & Inflammation, UMR 1173, Inserm, UVSQ/Université Paris Saclay, Montigny-le-Bretonneux, France.
Christophe HueInfection & Inflammation, UMR 1173, Inserm, UVSQ/Université Paris Saclay, Montigny-le-Bretonneux, France.
Anne BolandInfection & Inflammation, UMR 1173, Inserm, UVSQ/Université Paris Saclay, Montigny-le-Bretonneux, France.
Jean-François DeleuzeInfection & Inflammation, UMR 1173, Inserm, UVSQ/Université Paris Saclay, Montigny-le-Bretonneux, France.
Henri-Jean GarchonInfection & Inflammation, UMR 1173, Inserm, UVSQ/Université Paris Saclay, Montigny-le-Bretonneux, France.
Ilkay ErgençVIB Center for Inflammation Research, Ghent University Hospital, Ghent, Belgium.
Ann-Sophie De CraemerVIB Center for Inflammation Research, Ghent University Hospital, Ghent, Belgium.
Ulrike ErbenMedizinische Klinik für Gastroenterologie, Infektiologie und Rheumatologie, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
Thomas HäuplMedizinische Klinik für Rheumatologie und Klinische Immunologie, Campus Mitte, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Dirk ElewautVIB Center for Inflammation Research, Ghent University Hospital, Ghent, Belgium.
Maxime BrebanInfection & Inflammation, UMR 1173, Inserm, UVSQ/Université Paris Saclay, Montigny-le-Bretonneux, France.
Andreas GrützkauDeutsches Rheumaforschungszentrum (DRFZ), A Leibniz Institute, Berlin, Germany.
Uta SyrbeMedizinische Klinik für Gastroenterologie, Infektiologie und Rheumatologie, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, 12200, Berlin, Germany. uta.syrbe@charite.de.ORCID 0000-0001-8463-7890
Charité - Universitätsmedizin Berlin · DEInserm · FRGhent University Hospital · BEGerman Rheumatism Research Centre · DEFranklin University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn patients with axial spondyloarthritis (axSpA), monocytes show a pre-activated phenotype. Gut inflammation is a trigger of monocyte activation and may also affect their development in the bone marrow (BM). As gut inflammation is commonly observed in axSpA patients, we performed a detailed analysis of monocyte transcriptomes of axSpA patients in two cohorts and searched for signs of activation and developmental adaptations as putative imprints of gut inflammation.

methodsTranscriptomes of blood CD14

resultsTranscriptome analysis identified axSpA-specific monocyte signatures showing an imprint of LPS/cytokine-activated monocytes, late granulopoietic BM cells, blood neutrophils, and G-CSF-mobilized blood cells, which suggests LPS/TNF activation and more prominent BM adaptation promoting a neutrophil-like phenotype. GSEA mapped axSpA upregulated genes to inflammatory responses and TNFα signaling and downregulated probe-sets to metabolic pathways. Among translocation markers, LBP levels were significantly increased in axSpA patients vs. HC (p < 0.001). Stratified analysis by disease activity and stage identified an "active disease signature" (BASDAI ≥ 4) with an imprint of LPS/cytokine-activated monocytes and CD16

conclusionsThe neutrophil-like phenotype of axSpA monocytes points towards a biased monocytopoiesis from granulocyte-monocyte progenitors. This shift in monocytopoiesis and the LPS/cytokine imprint as well as the elevated LBP levels are indicators of systemic inflammation, which may result from bacterial translocation. The BM adaptation is most prominent in AS patients while disease activity appears to be linked to activation and trafficking of monocytes.

Indexed as

MonocytesSpondylarthritisCytokinesGene Expression ProfilingHumansTranscriptomeCytokinesGut translocationMonocytesSpondyloarthritisTranscriptomes

Identifiers

PMID34560894
PMCPMC8461951
OpenAlexW3200290972

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.