Evidence map›Paper›PMID 42398182›Full record

ArticleEBioMedicine2026

Multi-modal single-cell sequencing reveals network transition in circulating monocytes that aligns with faster recovery in patients with trauma and favours a response to M-CSF.

Tianmeng Chen, Julia Hughes, Julia Cornoy, Wei Chen, Richard Duerr, Timothy Billiar

Abstract read
In one paragraph

Article in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Tianmeng ChenDepartment of Surgery, University of Pittsburgh, Pittsburgh, PA, 15213, USA. Electronic address: tianmeng.chen@pitt.edu.
Julia HughesDepartment of Surgery, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
Julia CornoyDepartment of Surgery, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
Wei ChenDepartment of Pediatrics, University of Pittsburgh, Pittsburgh, PA, 15224, USA.
Richard DuerrDepartment of Medicine, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
Timothy BilliarDepartment of Surgery, University of Pittsburgh, Pittsburgh, PA, 15213, USA. Electronic address: billiar@pitt.edu.

Funding

Mechanisms of Immune Dysfunction after Trauma and Surgical SepsisR35GM127027 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TIMOTHY R BILLIAR · 2018 to 2026
$5.7M
High-Throughput Computing for Genomics and Bioinformatics ResearchS10OD028483 · OD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEE, ADRIAN V · 2021 to 2021
$574k
NIGMS NIH HHS R35 GM127027NIH HHS S10 OD028483
6 · The paper itself

Abstract

backgroundPrevious transcriptomic studies demonstrated an acute genomic storm in circulating immune cells after trauma that gradually returns to baseline. The magnitude and duration of these changes is associated with post-injury complications. We hypothesised that other immune cell features emerging in the subacute timeframe should be associated with recovery.

methodsWe applied DOGMA-seq on peripheral blood mononuclear cells isolated at day 3 after injury from the patients undergoing slow or fast recovery from critical illness (n = 8/group), along with age-and-sex matched healthy controls. We explored the functional responses of newly identified gene co-expression networks using in vitro cell culture (GM-CSF or M-CSF induced macrophage differentiation) followed by scRNA-seq.

findingsWe identified a subset of CD172a hi/MHCII hi, CD14+ monocytes that were distinct from baseline, and overrepresented in patients that recovered faster and associated with changes in several key gene co-expression networks. A gene co-expression pattern associated with chemotaxis and cell adhesion was overrepresented in patients with fast recovery and, specifically associated with increased accessibility of AP1 family motifs, continuously deviating from baseline, and favouring a response to M-CSF rather than GM-CSF during macrophage differentiation.

interpretationOur findings add a new information layer to the current paradigm by demonstrating that recovery is not simply a return to the baseline state and instead involves the emergence of new monocyte subset with new transcriptomic programs that may influence the macrophage response.

fundingNational Institutes of Health R35 grant R35GM127027 (T.B.).

Indexed as

Gene Regulatory NetworksMacrophage Colony-Stimulating FactorMonocytesSingle-Cell AnalysisWounds and InjuriesAdultCell DifferentiationFemaleGene Expression ProfilingHumansMacrophagesMaleMiddle AgedSingle-Cell Gene Expression AnalysisTranscriptomeMacrophage Colony-Stimulating FactorDOGMA-seqMacrophagesMonocytesscRNA-seqTrauma

Identifiers

PMID42398182
PMCPMC13351336

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.