Related Experiment Video
Updated: May 28, 2026

A Chemical Screening Procedure for Glucocorticoid Signaling with a Zebrafish Larva Luciferase Reporter System
Published on: September 10, 2013
The emerging role of C/EBPs in glucocorticoid signaling: lessons from the lung
1Respiratory Medicine Unit, Lung Research Laboratory L4:01, Department of Medicine, Karolinska Institutet, Karolinska University Hospital - Solna, 171 76 Stockholm, Sweden. abraham.roos@ki.se
Abstract:
Glucocorticoids (GCs) have been successfully used in the treatment of inflammatory diseases for decades. However, there is a relative GC resistance in several inflammatory lung disorders, such as chronic obstructive pulmonary disease (COPD), but still the mechanism(s) behind this unresponsiveness remains unknown. Interaction between transcription factors and the GC receptor contribute to GC effects but may also provide mechanisms explaining steroid resistance. CCAAT/enhancer-binding protein (C/EBP) transcription factors are important regulators of pulmonary gene expression and have been implicated in inflammatory lung diseases such as asthma, pulmonary fibrosis, cystic fibrosis, sarcoidosis, and COPD. In addition, several studies have indicated a role for C/EBPs in mediating GC effects. In this review, we discuss the different mechanisms of GC action as well as the function of the lung-enriched members of the C/EBP transcription factor family. We also summarize the current knowledge of the role of C/EBP transcription factors in mediating the effects of GCs, with emphasis on pulmonary effects, and their potential role in mediating GC resistance.
Insights
Glucocorticoids (GCs) treat inflammation but face resistance in lung diseases like COPD. CCAAT/enhancer-binding proteins (C/EBPs) may explain this steroid resistance by influencing GC effects in the lungs.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Immunology
Background:
- Glucocorticoids (GCs) are mainstays for inflammatory disease treatment.
- Steroid resistance is observed in lung disorders like COPD, with unknown mechanisms.
- Transcription factors interacting with the GC receptor may underlie resistance.
Purpose of the Study:
- To review glucocorticoid (GC) action mechanisms.
- To explore the function of lung-enriched CCAAT/enhancer-binding proteins (C/EBP).
- To summarize C/EBP roles in mediating GC effects and potential GC resistance in pulmonary diseases.
Main Methods:
- Literature review of GC mechanisms.
- Analysis of C/EBP family functions in lung biology.
- Synthesis of current knowledge on C/EBPs, GCs, and steroid resistance.
Main Results:
- GCs exert effects via receptor interactions.
- C/EBP transcription factors are key regulators of lung gene expression.
- C/EBPs are implicated in various inflammatory lung diseases and may mediate GC effects.
Conclusions:
- C/EBP transcription factors play significant roles in lung inflammation.
- Understanding C/EBP involvement is crucial for elucidating GC resistance mechanisms.
- Targeting C/EBPs could offer new therapeutic strategies for steroid-resistant lung diseases.
Related Concept Videos
Antiasthma Drugs: Inhaled Corticosteroids and Glucocorticoids
ICS work through a multifaceted mechanism of action. They suppress the inflammatory response caused by the proliferation of TH cells. They also reduce the transcription of the IL-2 gene, which is involved in the...
Cushing Syndrome II: Pathophysiology
COPD: Management Using Bronchodilators and Corticosteroids
Global Regulatory Systems
Cushing Syndrome I: Introduction
Cell Signaling in Plants