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Related Experiment Video

Updated: Jul 16, 2026

Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
08:27

Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury

Published on: May 21, 2018

Single-Cell and Spatial Transcriptomics Identify the Mono-S100A4 Subset Associated with Sepsis-Induced Lung Injury

Aihua Wang1,2,3, Chengfen Yin1,2,3, Yue Jin4,5

  • 1Central Hospital, Tianjin University, Tianjin, People's Republic of China.

Journal of Inflammation Research
|July 15, 2026
PubMed
Summary

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Sepsis-induced acute lung injury (ALI) involves monocyte immune dysregulation. A specific Mono-S100A4 subset, linked to the IL-17 pathway, may drive inflammation in septic ALI, warranting further study.

Area of Science:

  • Immunology
  • Pathophysiology
  • Computational Biology

Background:

  • Sepsis-induced immune dysregulation critically involves monocytes, which have dual pro-inflammatory and immunosuppressive roles.
  • The lungs are a primary target in sepsis, making monocyte dynamics crucial for understanding sepsis-induced acute lung injury (ALI).

Purpose of the Study:

  • To computationally characterize monocyte heterogeneity in sepsis-induced ALI using single-cell and spatial transcriptomics.
  • To identify specific monocyte subsets and their signaling pathways involved in ALI pathophysiology.
  • To experimentally validate findings in a mouse model of sepsis-induced ALI.

Main Methods:

  • Analysis of publicly available mouse single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) datasets.
Keywords:
Mono-S100A4acute lung injurymonocytescRNA-seqsepsisspatial transcriptomics

Related Experiment Videos

Last Updated: Jul 16, 2026

Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
08:27

Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury

Published on: May 21, 2018

  • Computational methods including cell-cell communication, trajectory analysis, and functional enrichment.
  • Experimental validation using a mouse model of sepsis-induced ALI with histological, molecular, and protein analyses.

    • Main Results:

    • Clustering revealed a restructured immune landscape with monocyte accumulation in septic ALI, primarily in bronchial regions.
    • A distinct Mono-S100A4 monocyte subset was identified, showing enhanced intercellular communication via the MIF-(CD74+CD44) axis.
    • Mono-S100A4 enrichment in the IL-17 signaling pathway and Th17 cell differentiation was observed, with in vivo validation showing increased S100A4, IL-17A, MIF, and CD74 in septic ALI mouse lungs.

    Conclusions:

    • The Mono-S100A4 subset is associated with Th17 pathway activation through the MIF-(CD74+CD44) axis.
    • This suggests a potential pathogenic role for Mono-S100A4 in sepsis-induced ALI.
    • Further functional experiments are needed to validate this hypothesis.