ArticleNature communications2023
Single cell transcriptomics identifies distinct profiles in pediatric acute respiratory distress syndrome.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 18 citations in OpenAlex.
- Development and validation of a machine learning-driven framework for differentiating pediatric bronchopneumonia from lobar pneumonia: a multicenter investigation.European journal of medical research · 2025Trial
- Article
- Ferroptosis-Senescence Crosstalk in Sepsis-Associated Acute Lung Injury: Mechanisms and Therapeutic Opportunities.Biomedicines · 2026Review
- The Acute Respiratory Distress Syndrome (ARDS): epidemiology, etiology, molecular mechanisms, diagnosis and therapeutic strategies.Molecular biomedicine · 2026Review
- FOLR3+neutrophils contribute to sepsis by exacerbating hyper-inflammation.Genes and immunity · 2026Article
- The landscape of protein post-translational modifications in the pathogenesis of acute respiratory distress syndrome.Journal of thoracic disease · 2026Review
- A high dimensionality approach reveals immunopathogenic responses driving severe pediatric acute respiratory distress syndrome.Nature communications · 2026Article
- Macrophages orchestrate antiviral defense and epithelial repair in a human iPSC-derived alveolar air-liquid interface.JCI insight · 2026Article
- Distinct Blood and Lung Proteins Drive Pulmonary Capillary Leak in Children With Severe Hypoxemic Respiratory Failure.Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies · 2026Observational
- Unique nasal cell states induced by common pediatric respiratory viruses.bioRxiv : the preprint server for biology · 2026Article
- Analysis of the epidemic situation of respiratory pathogens in central and southern China before and after the COVID-19 pandemic.Frontiers in pediatrics · 2026Article
- Lipoxin A4 AttenuatesJournal of inflammation research · 2026Article
- Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.Frontiers in cell and developmental biology · 2026Review
- Biomarkers for Pediatric Acute Respiratory Distress Syndrome: A Systematic Review.Journal of inflammation research · 2026Review
- Multi-omics analysis reveals distinct spatial compartmentalization of lung repair niches in pediatric ARDS.Journal of translational medicine · 2025Article
- High expression of interleukin-18 receptor alpha correlates with severe respiratory viral disease and defines T cells with reduced cytotoxic signatures.Nature communications · 2025Article
- Article
- Transcriptomic signatures of neonatal acute respiratory distress syndrome in a prospective cohort of respiratory distress.iScience · 2025Article
- Defining the host dependencies and the transcriptional landscape of RSV infection and bystander activation.bioRxiv : the preprint server for biology · 2025Article
- New perspectives on extracorporeal life support: expert teams and precise selection of candidates are transforming pediatric cancer and hematopoietic cell transplantation care.Frontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Acute respiratory distress syndrome (ARDS), termed pediatric ARDS (pARDS) in children, is a severe form of acute respiratory failure (ARF). Pathologic immune responses are implicated in pARDS pathogenesis. Here, we present a description of microbial sequencing and single cell gene expression in tracheal aspirates (TAs) obtained longitudinally from infants with ARF. We show reduced interferon stimulated gene (ISG) expression, altered mononuclear phagocyte (MNP) transcriptional programs, and progressive airway neutrophilia associated with unique transcriptional profiles in patients with moderate to severe pARDS compared to those with no or mild pARDS. We additionally show that an innate immune cell product, Folate Receptor 3 (FOLR3), is enriched in moderate or severe pARDS. Our findings demonstrate distinct inflammatory responses in pARDS that are dependent upon etiology and severity and specifically implicate reduced ISG expression, altered macrophage repair-associated transcriptional programs, and accumulation of aged neutrophils in the pathogenesis of moderate to severe pARDS caused by RSV.
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Registered trials
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.