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Related Concept Videos

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.

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Updated: May 13, 2026

Label-free Neutrophil Enrichment from Patient-derived Airway Secretion Using Closed-loop Inertial Microfluidics
07:37

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Neutrophil elastase-mediated lung disease.

Robert A Sandhaus1, Gerard Turino

  • 1National Jewish Health, Denver, Colorado 80206, USA.

COPD
|March 27, 2013
PubMed
Summary

Neutrophil and macrophage elastases contribute to lung disease. Alpha-1 antitrypsin deficiency disrupts protease-anti-protease balance, increasing the risk of destructive lung conditions.

Area of Science:

  • Biochemistry
  • Pulmonology
  • Immunology

Background:

  • Neutrophil and macrophage elastases are implicated in lung disease initiation and progression.
  • The lung's elastin-rich connective tissue is susceptible to elastolytic proteases.
  • Neutrophil elastase aids neutrophil migration and protein degradation during inflammation.

Purpose of the Study:

  • To explore the role of elastases in lung disease.
  • To understand the protective function of protease inhibitors.
  • To examine the consequences of protease-anti-protease imbalance in alpha-1 antitrypsin deficiency.

Main Methods:

  • This study is a review of existing literature and biological mechanisms.
  • It analyzes the function of neutrophil elastase and its inhibitors.

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  • It discusses the implications of alpha-1 antitrypsin deficiency.

    • Main Results:

    • Elastases can damage lung tissue, particularly the elastin-rich framework.
    • Protease inhibitors, like alpha-1 antitrypsin, protect lung tissue from elastolytic damage.
    • Alpha-1 antitrypsin deficiency disrupts this balance, leading to increased lung disease risk.

    Conclusions:

    • The protease-anti-protease balance is crucial for maintaining lung health.
    • Dysregulation of this balance, as seen in alpha-1 antitrypsin deficiency, significantly elevates the risk of destructive lung diseases.
    • Understanding these mechanisms is key to developing therapeutic strategies for lung conditions.