Evidence map›Paper›PMID 41888646›Full record

ArticleMolecular medicine (Cambridge, Mass.)2026

Preterm birth skews the developmental trajectory of myeloid-derived suppressor cells in the first 48 hours of life: single-cell transcriptomics and inferred intercellular communication.

Miguel Hernández-Ríos, Jaimar Rincon, Leandro Balzano-Nogueira, Valerie Polcz, Dayuan Wang, Whitman Wiggins, Christine Rodhouse, Athina Yoham, Feifei Xiao, Ricardo Ungaro and 6 more

Abstract read
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In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

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No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

16 authors.

Miguel Hernández-Ríos *Sepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Jaimar Rincon *Sepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA. jaimar.rincon@surgery.ufl.edu.ORCID 0000-0002-4611-106X
Leandro Balzano-NogueiraSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Valerie PolczSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Dayuan WangDepartment of Biostatistics, University of Florida Colleges of Medicine and Public Health and Health Sciences, Gainesville, Florida, USA.
Whitman WigginsSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Christine RodhouseSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Athina YohamSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Feifei XiaoSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Ricardo UngaroSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Marvin DirainSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Lyle MoldawerSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Robert MaileSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Guoshuai CaiSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Philip EfronSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Shawn LarsonSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.

Funding

R35 Equipment SupplementR35GM140806 · NIGMS · UNIVERSITY OF FLORIDA · PI EFRON, PHILIP A · 2021 to 2025
$2.2M
National Institutes of Health, United States R01GM143143NIH HHS R35GM140806
6 · The paper itself

Abstract

backgroundPrematurity is a leading cause of neonatal and childhood mortality, with infections driving early deaths. Innate immunity provides frontline defense after birth and is shaped in part by myeloid-derived suppressor cells (MDSCs). The role of MDSCs in regulation of neonatal immunity, especially in the context of prematurity, remains elusive. We sought to understand the transcriptional landscape of neonatal immune myeloid regulators, specifically differences between preterm and full-term neonates. Insight into specific cellular networks could help understand how to skew preterm MDSCs’ development towards classical immunotolerant and anti-microbial mechanisms.

methodsThis cross-sectional study used single-cell RNA sequencing to characterize the neonatal MDSC transcriptional landscape, developmental trajectories, and predicted signaling networks within 48 h after birth. Peripheral blood mononuclear cells were isolated from 7 preterm neonates (< 36 weeks gestational age), 6 full-term neonates (> 37 weeks), and 6 healthy adult (21–45 years old, control). Primary exposure was premature birth and neonatal intensive care hospitalization from a single-center, academic tertiary care hospital between 2023 – 2024.

resultsAmong ~ 339,000 cells, preterm neonates exhibited enrichment of polymorphonuclear MDSCs (10.6% ± 5.3%) vs full-term (2.6% ± 1.3%) and adults (0.4% ± 1.3%). Trajectory analysis identified a prematurity-associated differentiation branch characterized by inflammatory signaling, mitochondrial stress, and heightened protein-translation programs, distinct from a conserved, tolerogenic MDSC trajectory present across ages. Cell-communication modeling showed intensified outgoing and incoming signaling via ADGRE, RESISTIN, TGF-β, ANNEXIN, and ICAM networks. Antigen presentation signatures suggested preserved MHC-I output and diminished MHC-II interactions in neonates, with increased MHC-I input to preterm polymorphonuclear MDSCs.

conclusionsPrematurity is associated with early divergence of MDSC maturation toward an inflammatory and metabolically stressed PMN-MDSC state with altered immune communication. These findings identify cellular mechanisms that may contribute to the heightened tissue damage and infection susceptibility of preterm neonates and highlight MDSC signaling as a potential target for early-life immunomodulatory interventions.

Indexed as

Cell CommunicationMyeloid-Derived Suppressor CellsPremature BirthTranscriptomeAdultCross-Sectional StudiesFemaleGene Expression ProfilingHumansInfant, NewbornInfant, PrematureMaleSingle-Cell AnalysisSingle-Cell Gene Expression AnalysisCell communicationDevelopmental trajectoryMyeloid-derived suppressor cellsPreterm neonatesSingle-cell RNA sequencing

Identifiers

PMID41888646
PMCPMC13147740

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