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Updated: Jun 3, 2026

A Data-Driven Approach to Quantifying Immune States in Sepsis

A Data-Driven Approach to Quantifying Immune States in Sepsis

Published on: February 7, 2025

Gene expression in human sepsis: what have we learned?

James A Russell¹

¹Critical Care Medicine, St, Paul's Hospital, 1081 Burrard Street, Vancouver, BC, Canada V6Z 1Y6. jim.russell@hli.ubc.ca

Critical Care (London, England)

|March 12, 2011

Summary

A systematic review found no clear shift from pro- to anti-inflammatory gene expression in human sepsis blood. Upregulation of pathogen recognition and signaling pathways was consistent, but study variations limit definitive conclusions on sepsis phenotypes.

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Last Updated: Jun 3, 2026

A Data-Driven Approach to Quantifying Immune States in Sepsis

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Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

Area of Science:

* Critical Care Medicine
* Molecular Biology
* Immunology

Background:

* Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.
* The traditional view posits a shift from a pro-inflammatory to an anti-inflammatory phenotype during sepsis progression.
* Gene expression studies in sepsis aim to elucidate these dynamic host responses.

Purpose of the Study:

* To systematically review gene expression in blood from human sepsis patients.
* To assess the evidence for a transition in inflammatory gene expression phenotypes during sepsis.
* To identify consistent patterns and limitations in existing sepsis gene expression research.

Main Methods:

* Systematic review of 12 studies on gene expression in human sepsis blood.
* Defined screening, inclusion, and quality assessment criteria for studies.
* Analysis focused on gene expression patterns, particularly inflammatory markers.

Main Results:

* No discernible transition from pro-inflammatory to anti-inflammatory gene expression phenotype was observed in sepsis blood.
* Consistent upregulation of pathogen recognition receptors and signal transduction pathways was noted across studies.
* Significant heterogeneity in study designs, timing, tissue types, and sepsis causes complicates interpretation.

Conclusions:

* Current gene expression data do not strongly support the paradigm of a distinct pro- to anti-inflammatory phenotype shift in sepsis.
* Variability in study methodologies (e.g., time of blood draw, tissue heterogeneity, microbial causes) limits definitive conclusions.
* Further well-designed studies are needed to clarify sepsis-induced gene expression dynamics and validate findings.