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Related Concept Videos

Chronic Obstructive Pulmonary Disease I: Introduction01:23

Chronic Obstructive Pulmonary Disease I: Introduction

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

Chronic Obstructive Pulmonary Disease-I: Introduction

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.
Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
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...

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Updated: May 26, 2026

Measurement of Chitinase Activity in Biological Samples
03:32

Measurement of Chitinase Activity in Biological Samples

Published on: August 22, 2019

Genetic association between human chitinases and lung function in COPD.

F Aminuddin1, L Akhabir, D Stefanowicz

  • 1James Hogg Research Centre, Providence Heart and Lung Institute, St. Paul's Hospital, The University of British Columbia, 1081 Burrard Street, Vancouver, BC V6Z 1Y6, Canada.

Human Genetics
|December 28, 2011
PubMed
Summary
This summary is machine-generated.

Genetic variations in human chitinase genes (AMCase and CHIT1) impact lung function and its decline in COPD patients. However, these genetic associations did not consistently predict COPD status across different populations.

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Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity
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Last Updated: May 26, 2026

Measurement of Chitinase Activity in Biological Samples
03:32

Measurement of Chitinase Activity in Biological Samples

Published on: August 22, 2019

Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity
07:13

Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity

Published on: January 6, 2015

Area of Science:

  • Immunology
  • Genetics
  • Pulmonology

Background:

  • Two primary human chitinases, acid mammalian chitinase (AMCase) and chitotriosidase (CHIT1), are known to influence host immune responses.
  • Genetic variations in these chitinases may play a role in the pathogenesis of chronic obstructive pulmonary disease (COPD).

Purpose of the Study:

  • To investigate the association between genetic variations in chitinase genes (AMCase and CHIT1) and phenotypes related to COPD.
  • To analyze the relationship between specific chitinase gene polymorphisms and lung function parameters, including FEV(1) decline.

Main Methods:

  • Polymorphisms in chitinase genes were selected based on prior associations with respiratory diseases.
  • Associations with lung function and FEV(1) decline were analyzed in the Lung Health Study (LHS) cohort.
  • Associations with COPD affection status were tested in four additional COPD case-control populations.

Main Results:

  • In the Caucasian LHS cohort, AMCase rs3818822 polymorphism (GG genotype) was associated with higher AMCase protein and chitinase activity, and significantly different baseline FEV(1).
  • CHIT1 rs2494303 polymorphism showed a significant association with the rate of FEV(1) decline in the LHS cohort.
  • In the African American LHS population, CHIT1 rs2494303 and AMCase G339T genotypes were linked to FEV(1) decline.

Conclusions:

  • Chitinase gene variants significantly influence lung function levels and decline in the LHS cohort.
  • The study could not replicate the association between chitinase gene alleles and COPD affection status in independent COPD case-control populations.