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Related Experiment Video

Updated: Oct 13, 2025

Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
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Development of Exhausted Memory Monocytes and Underlying Mechanisms.

Kisha Pradhan1, Ziyue Yi2, Shuo Geng1

  • 1Department of Biological Sciences, Virginia Tech, Blacksburg, VA, United States.

Frontiers in Immunology
|November 15, 2021
PubMed
Summary

Repetitive lipopolysaccharide (LPS) challenges generate exhausted monocytes in sepsis models. STAT1, via TRAM, drives this exhaustion, offering new therapeutic targets for sepsis-induced immune dysfunction.

Keywords:
CD38TRAMexhaustionmonocyte memorypathogenic inflammation

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Area of Science:

  • Immunology
  • Cell Biology
  • Sepsis Pathophysiology

Background:

  • Exhausted monocytes, characterized by inflammation and immunosuppression, are key in sepsis.
  • Mechanisms driving monocyte exhaustion in sepsis remain poorly understood.

Purpose of the Study:

  • To investigate the generation and underlying mechanisms of exhausted monocytes using a murine sepsis model.
  • To identify key molecular players involved in LPS-induced monocyte exhaustion.

Main Methods:

  • Primary murine monocytes were subjected to prolonged, repetitive lipopolysaccharide (LPS) challenges.
  • Phenotypic analysis using Ly6C expression and single-cell RNA sequencing (scRNAseq) was performed.
  • Molecular pathways including STAT1, TRAM, CD38, NAD+, ROS, and mitochondrial respiration were assessed.

Main Results:

  • Repetitive LPS exposure skewed monocytes to the Ly6Chi exhausted phenotype, mirroring human sepsis.
  • scRNAseq revealed expanded Ly6Chi monocytes with elevated inflammatory genes.
  • CD38 was identified as an inflammatory mediator linked to NAD+ depletion, ROS elevation, and impaired mitochondrial function.
  • STAT1 activation, dependent on the TRAM adaptor of the TLR4 pathway, was crucial for LPS-induced monocyte exhaustion.

Conclusions:

  • This study elucidates the generation of exhausted monocytes in sepsis, highlighting the roles of CD38 and STAT1.
  • TRAM-dependent STAT1 activation is a critical mechanism driving monocyte exhaustion.
  • Targeting the TRAM-STAT1 axis may offer novel therapeutic strategies for sepsis.