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Related Experiment Video

Updated: Jan 28, 2026

Endotoxin Activity Assay for the Detection of Whole Blood Endotoxemia in Critically Ill Patients

Endotoxin Activity Assay for the Detection of Whole Blood Endotoxemia in Critically Ill Patients

Published on: June 24, 2019

RelB sustains IkappaBalpha expression during endotoxin tolerance.

Xiaoping Chen¹, Barbara K Yoza, Mohamed El Gazzar

¹Department of Internal Medicine, Section of Molecular Medicine, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. xchen@wfubmc.edu

Clinical and Vaccine Immunology : CVI

|November 21, 2008

Summary

This summary is machine-generated.

The transcription factor RelB plays a dual role in regulating immune responses. It represses pro-inflammatory genes and activates anti-inflammatory genes during severe systemic inflammation and endotoxin tolerance.

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Area of Science:

Immunology
Molecular Biology
Epigenetics

Background:

Severe systemic inflammation (SSI) induces epigenetic modifications in leukocytes, altering gene expression.
Lipopolysaccharide (LPS)-induced endotoxin tolerance in THP-1 cells mimics these changes.
Previously, RelB was shown to repress pro-inflammatory genes like IL-1beta and TNF-alpha.

Purpose of the Study:

To investigate the role of RelB in regulating anti-inflammatory genes during LPS tolerance.
To examine RelB's function in human SSI.

Main Methods:

Utilized the THP-1 cell model of LPS endotoxin tolerance.
Analyzed RelB binding to the IkappaBalpha promoter.
Investigated RelB binding to IkappaBalpha in leukocytes from human SSI patients.

Main Results:

RelB is required for sustained expression of the anti-inflammatory gene IkappaBalpha in LPS-tolerant THP-1 cells.
RelB binds to the IkappaBalpha promoter with NF-kappaB p50, involving a dimer exchange with p65.
RelB also binds to the IkappaBalpha promoter in leukocytes from human SSI patients.

Conclusions:

RelB acts as a dual transcription regulator in innate immunity.
RelB activates anti-inflammatory genes (IkappaBalpha) and represses pro-inflammatory genes (IL-1beta, TNF-alpha).
These findings elucidate RelB's complex role in immune homeostasis during inflammation and tolerance.