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Integrated transcriptomic and proteomic profiling identifies an interferon-dependent inflammatory endotype in sepsis.

Andrian Fratea1, Anca-Lelia Riza2, Florentina Dumitrescu3

  • 1Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen 6500 HB, the Netherlands; Human Genomics Laboratory, Functional Genomics Group, University of Medicine and Pharmacy of Craiova, Craiova 200349, Romania.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|January 20, 2026
PubMed
Summary

Sepsis patient immune responses vary by inflammatory endotype, not infection site. High-inflammatory sepsis shows activated interferon-gamma, CXCL9, and CXCL10, suggesting personalized immunotherapy targets.

Keywords:
EndotypeInnate immunityInterferonOmicsProteomicsSepsisTranscriptomics

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Area of Science:

  • Genomics
  • Immunology
  • Translational Medicine

Background:

  • Sepsis is a leading cause of global mortality, complicated by patient heterogeneity.
  • Improved sepsis outcomes require patient stratification into distinct endotypes.
  • This study explores sepsis transcriptomics based on inflammatory endotypes.

Purpose of the Study:

  • To investigate the transcriptomic differences in sepsis patients stratified by inflammatory endotype.
  • To identify key immune pathways and gene expression patterns associated with sepsis severity.
  • To explore potential targets for personalized sepsis immunotherapies.

Main Methods:

  • Peripheral blood mononuclear cells from 125 sepsis patients and 299 controls were analyzed.
  • RNA sequencing identified differentially expressed genes and enriched pathways.
  • Transcriptomic profiles were compared between "high-" and "low-inflammatory" endotypes.

Main Results:

  • Sepsis induced broad changes in innate immunity genes (phagocytosis, antimicrobial peptides) and reduced NK cell immunity.
  • Adaptive immunity genes, including T cell differentiation markers, were downregulated.
  • High-inflammatory sepsis showed upregulated interferon-associated chemokines (CXCL9, CXCL10) in cells and serum.

Conclusions:

  • Sepsis immune dysregulation is primarily driven by disease severity, not infection site.
  • The interferon-gamma-CXCL9-CXCL10 axis in high-inflammatory sepsis is a potential target for personalized immunotherapies.