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Related Experiment Video

Updated: May 26, 2026

A Data-Driven Approach to Quantifying Immune States in Sepsis
07:42

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Published on: February 7, 2025

Metabolic and post-translational modifications in sepsis-associated immune dysfunction: a conceptual framework.

Mingze Xu1, Ziye Zhang1, Min Zhu2

  • 1Department of Emergency Surgery, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China.

Frontiers in Immunology
|May 25, 2026
PubMed
Summary

Sepsis immune collapse involves a metabolic-PTM temporal switch model, where post-translational modifications (PTMs) and metabolism rewire immune signaling. This explains why immune stimulation fails in late sepsis.

Keywords:
epigenetic regulationimmunosuppressionmetabolic signalingpost-translational modificationsepsis

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Area of Science:

  • Immunology
  • Molecular Biology
  • Systems Biology

Background:

  • Sepsis involves immune signal transduction collapse.
  • Post-translational modifications (PTMs) regulate immune response dynamics.
  • The shift from cytokine storm to immune paralysis in sepsis is poorly understood at a molecular level.

Purpose of the Study:

  • To propose a metabolic-PTM temporal switch model for sepsis-induced immune dysfunction.
  • To explain the molecular logic behind the transition in immune signaling during sepsis.
  • To provide a framework for understanding context-dependent immune dysfunction and intervention outcomes.

Main Methods:

  • Conceptual modeling integrating PTMs, cellular metabolism, and chromatin structure.
  • Analysis of PTM patterns (phosphorylation, ubiquitination, lactylation) across sepsis stages.
  • Consideration of metabolic availability and chromatin accessibility as constraints on signaling.

Main Results:

  • A model is proposed where immune signaling is rewired by PTM configurations influenced by metabolism and chromatin.
  • Early sepsis: Permissive metabolism and open chromatin favor reversible PTMs amplifying innate immunity.
  • Late sepsis: Metabolic stress and chromatin condensation promote persistent PTMs, leading to immune refractoriness.

Conclusions:

  • The metabolic-PTM temporal switch model explains immune dysfunction in sepsis as a loss of signaling competence, not just attenuation.
  • This framework clarifies why immune stimulation often fails in late-stage sepsis due to impaired signaling architecture.
  • Understanding context-associated PTM patterns offers guidance for interpreting sepsis outcomes and designing interventions.