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pmid:41114487
Single-Cell Profiling Identifies JUNB/SPI1-Driven Inflammatory Programs and Novel Communication Axes in Myeloid Cells of Sepsis.
Liyao Liu · Lin Zhao · Jixiang Tan
Endocrine, metabolic & immune disorders drug targets · 2025 doi:10.2174/0118715303425071250925075308
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Experiment
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Data
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Analysis
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Complete file
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We aimed to characterize infiltrating cells in sepsis and provide novel insight for the treatment of sepsis.\nMATERIALS AND METHODS: Whole-blood scRNA-seq samples from four septic patients and five healthy subjects were collected from the Gene Expression Omnibus (GEO) database (GSE175453). The Seurat R package was used for quality control and cell clustering by scRNA- seq analysis. Gene set enrichment analysis (GSEA) was performed using the clusterProfiler R package for pathway enrichment analysis. Then, the SCENIC analysis was used to identify key transcriptional regulons, and the CellChat R package was used for cell communication analysis.\nRESULTS: We mainly obtained 9 cell clusters, including myeloid cells, T cells, dendritic cells, NKT cells, B cells, plasma B cells, megakaryocytes, mast cells and erythrocytes. Notably, myeloid cells, erythrocytes and mast cells had a higher proportion in sepsis patients. Activated IL-17 and p53 pathways supported anti-infection response in myeloid cells, and JUNB and SPI1 mediated multiple inflammatory pathways, including TNF signaling and neutrophil activation. We also identified that the cell interaction mode of myeloid cells, such as MPZL1-MPZL1 and FASL-FAS, may serve as a potential target for an anti-inflammatory response in sepsis treatment.\nDISCUSSIONS: The scRNA-seq analysis revealed pro-inflammatory pathways (IL-17, p53) and key regulators (JUNB, SPI1) in septic myeloid cells. 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