Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

5.3K
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
5.3K
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

21
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...
21
Chronic Obstructive Pulmonary Disease I: Introduction01:23

Chronic Obstructive Pulmonary Disease I: Introduction

3
Chronic obstructive pulmonary disease is a common, preventable, and treatable respiratory disorder characterized by persistent symptoms and progressive airflow limitation. This limitation results from a combination of small-airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), both driven by chronic inflammation from exposure to harmful particles or gases.The disease includes two main pathological entities: emphysema, marked by destruction of alveolar walls and...
3
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

2.3K
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...
2.3K
Chronic Obstructive Pulmonary Disease-I: Introduction01:20

Chronic Obstructive Pulmonary Disease-I: Introduction

4.3K
Chronic Obstructive Pulmonary Disease (COPD) is a long-lasting respiratory condition requiring continuous attention and care. It is a progressive lung disease that leads to breathing challenges due to airflow obstruction. It manifests as persistent respiratory symptoms and restricted airflow resulting from abnormalities in the airways and alveoli, usually due to long-term exposure to harmful particles or gases. COPD mainly consists of two primary conditions: emphysema and chronic bronchitis.
4.3K
Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.01:25

Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.

4.2K
Understanding the variety of primary symptoms and systemic complications that characterize chronic obstructive pulmonary disease (COPD) is crucial for healthcare professionals.
Symptoms of COPD can be classified as primary or systemic. Primary symptoms relate to reduced airflow, while systemic or extrapulmonary symptoms relate to COPD's broader impact on the body.
Primary Symptoms of COPD:
4.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Does a Digital Prehabilitation Solution Informed by Evidence-Based Interventions Reduce the Healthcare Burden and Improve Outcomes for Patients Awaiting Cardiac Surgery?-A Systematic Review.

Heart, lung & circulation·2026
Same author

Peripheral Blood Inflammatory Markers and Immune Cell Profiles in Smokers With and Without COPD.

Pulmonary therapy·2026
Same author

Examining the benefits of industry clinical placements for medical laboratory science academics.

Laboratory medicine·2026
Same author

Extracellular vimentin promotes neutrophil-dominant granulomatous inflammation in progressive pulmonary sarcoidosis.

Clinical science (London, England : 1979)·2026
Same author

Carnosine augments the efficacy of pulmonary rehabilitation in COPD: insights from a preclinical model.

Clinical science (London, England : 1979)·2026
Same author

Immunogenicity of high-dose recombinant influenza vaccine versus standard-dose egg-grown and cell-grown vaccines among frequently and infrequently vaccinated young adults in Singapore: a randomised, controlled, double-blind, single-centre, phase 4 clinical trial.

The Lancet. Infectious diseases·2026

Related Experiment Video

Updated: Apr 19, 2026

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation
07:40

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation

Published on: August 30, 2019

9.6K

Targeting pro-resolution pathways to combat chronic inflammation in COPD.

Steven Bozinovski1, Desiree Anthony1, Ross Vlahos1

  • 1Lung Health Research Centre, Department of Pharmacology and Therapeutics, The University of Melbourne, Parkville 3010, Australia.

Journal of Thoracic Disease
|December 6, 2014
PubMed
Summary

Chronic obstructive pulmonary disease (COPD) involves persistent inflammation due to failed resolution. New therapies targeting the ALX/FPR2 receptor may promote healing in COPD airways.

Keywords:
ALX/FPR2Serum Amyloid A (SAA)catabasischronic obstructive pulmonary disease (COPD)inflammationresolution

More Related Videos

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
08:17

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

Published on: August 25, 2017

11.7K
Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

8.3K

Related Experiment Videos

Last Updated: Apr 19, 2026

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation
07:40

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation

Published on: August 30, 2019

9.6K
Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
08:17

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

Published on: August 25, 2017

11.7K
Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

8.3K

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Pharmacology

Background:

  • Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow obstruction and persistent airway inflammation.
  • Despite excessive inflammation, COPD airways are prone to microbial colonization and exacerbations, leading to tissue damage.
  • Key inflammatory mediators like CXCL8 (IL-8) and leukotriene B4 (LTB4) are overproduced, while macrophage clearance of pathogens and apoptotic cells is inefficient.

Purpose of the Study:

  • To explore why pro-resolution mediators fail to resolve inflammation in COPD.
  • To investigate the role of the G-protein coupled receptor ALX/FPR2 in COPD pathogenesis.
  • To identify therapeutic opportunities by targeting ALX/FPR2 conformations.

Main Methods:

  • Review and synthesis of existing literature on COPD inflammation and resolution pathways.
  • Focus on the function of pro-resolving mediators (lipoxin A4, D-series resolvins, Annexin A1) and their interaction with ALX/FPR2.
  • Analysis of how airway mediators like Serum Amyloid A (SAA) and LL-37 activate ALX/FPR2.

Main Results:

  • Pro-resolution mediators are ineffective in switching off inflammation in COPD, despite converging on ALX/FPR2.
  • ALX/FPR2 is activated by various mediators present in COPD airways, including SAA and LL-37.
  • Evidence suggests ALX/FPR2 exhibits agonist-biased conformations, leading to diverse functional outcomes.

Conclusions:

  • Therapeutic strategies could involve developing stable pro-resolving analogs to modulate ALX/FPR2 conformations.
  • Targeting specific ALX/FPR2 conformations may counteract pathogenic signaling in COPD.
  • Promoting non-phlogistic clearance pathways via ALX/FPR2 modulation is crucial for inflammation resolution in COPD.