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Related Concept Videos

Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

Chronic obstructive pulmonary disease (COPD) is a group of lung conditions that progressively worsen over time, including chronic bronchitis and emphysema. This cluster of diseases collectively leads to a gradual and irreversible decline in lung function over time.
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
Co-activators and Co-repressors02:04

Co-activators and Co-repressors

Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.01:25

Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.

Understanding the variety of primary symptoms and systemic complications that characterize chronic obstructive pulmonary disease (COPD) is crucial for healthcare professionals.
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Primary Symptoms of COPD:

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Related Experiment Video

Updated: May 23, 2026

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification
10:21

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Published on: September 20, 2024

Reduced nuclear factor-κB repressing factor: a link toward systemic inflammation in COPD.

Kang-Yun Lee1, Shu-Chuan Ho, Yao-Fei Chan

  • 1Dept of Thoracic Medicine Chang Gung Memorial Hospital, Chang Gung University College of Medicine, 199 Tun-Hwa North Road, Taipei, Taiwan.

The European Respiratory Journal
|March 24, 2012
PubMed
Summary
This summary is machine-generated.

Nuclear factor (NF)-κB repressing factor (NRF) is reduced in COPD patients, increasing interleukin (IL)-8/CXCL8 production. This impairment in NRF function may drive chronic systemic inflammation in COPD.

Related Experiment Videos

Last Updated: May 23, 2026

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification
10:21

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Published on: September 20, 2024

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Molecular Biology

Background:

  • Chronic systemic inflammation is linked to COPD manifestations and mortality.
  • The role of Nuclear Factor (NF)-κB Repressing Factor (NRF) in human diseases, particularly COPD, remains unexplored.

Purpose of the Study:

  • To investigate the hypothesis that impaired NRF regulatory mechanisms in COPD peripheral blood mononuclear cells (PBMCs) lead to excessive Interleukin (IL)-8/CXCL8 production.
  • To assess NRF expression, NF-κB activation, IL-8/CXCL8 release, and intracellular oxidative stress in PBMCs from normal subjects and stable COPD patients.

Main Methods:

  • Assessed NRF expression, NF-κB activation, IL-8/CXCL8 release, and oxidative stress in PBMCs.
  • Utilized primary PBMCs with NRF overexpression, NRF knockdown, and H2O2 exposure to elucidate mechanisms.

Main Results:

  • Stable COPD patients exhibited decreased NRF expression and enhanced NF-κB activation and IL-8/CXCL8 release in PBMCs compared to normal subjects.
  • Reduced NRF and increased RNA polymerase II occupancy were observed at the IL-8/CXCL8 promoter in COPD PBMCs.
  • NRF knockdown increased IL-8/CXCL8 production, while NRF overexpression attenuated it in normal PBMCs.
  • Increased intracellular oxidative stress was noted in COPD PBMCs, with H2O2 exacerbating NRF reduction and IL-8/CXCL8 production.

Conclusions:

  • NRF expression is reduced in PBMCs of stable COPD patients, likely due to oxidative stress.
  • This NRF reduction leads to increased IL-8/CXCL8 production, potentially contributing to chronic systemic inflammation in COPD.