Chest
Mechanisms in COPD: Differences From Asthma
Section snippets
Inflammatory Cells and Pathology
Airway inflammation in asthma is characterized by an eosinophilic inflammation, with an increase in activated and degranulating eosinophils in bronchial biopsies, BAL, and in induced sputum.12 There is also an increase in CD4+ T lymphocytes (T-helper type 2 cells) that appear to orchestrate the eosinophilic inflammation and degranulated mast cells that underlie the rapid and episodic bronchoconstrictor responses that are so characteristic of asthma. Epithelial shedding is a common feature of
Inflammatory Mediators
More than 50 inflammatory mediators have been implicated in asthma.11 Cysteinyl-leukotrienes are prominent bronchoconstrictors in asthma and are derived from mast cells and eosinophils. Histamine, prostaglandins, and kinins may also contribute to bronchoconstriction in asthma. Cholinergic reflexes may be activated by these inflammatory mediators, particularly kinins. β2-Agonists are by far the most effective bronchodilators in asthma, as they act as functional antagonists and counteract the
Enzymes
Several inflammatory enzymes are involved in asthma.11 Mast cell tryptase may play an important role in AHR and in some aspects of airway remodeling in asthma. In COPD, there is excessive activity of proteases, and an imbalance between proteases and endogenous antiproteases. Several proteases are likely to be involved in lung parenchymal destruction. Neutrophil elastase, a neutral serine protease, is a major constituent of lung elastolytic activity and also potently stimulates mucus secretion.
Response to Anti-inflammatory Treatment
The response to treatment differs markedly between asthma and COPD. The eosinophilic inflammation in asthma is markedly suppressed by corticosteroids, which inhibit almost every aspect of the inflammatory process.25 There is a disappearance of eosinophils from the airways and sputum, with a reduction in AHR. In contrast, corticosteroids do not appear to have any effect on the inflammation in COPD, with no changes in neutrophilic inflammation, reduction in inflammatory mediators, or proteases.26
References (30)
- et al.
Airway inflammation in COPD assessed by sputum levels of interleukin-8
Chest
(1997) - et al.
Cloning and characterization of a unique elastolytic metalloproteinase produced by human alveolar macrophages
J Biol Chem
(1993) Chronic obstructive pulmonary disease: new opportunities for drug development
Trends Pharmacol Sci
(1998)Pathophysiology of asthma
Br J Clin Pharmacol
(1996)Structural and inflammatory changes in COPD: a comparison with asthma
Thorax
(1998)- et al.
Activated T-lymphocytes and macrophages in bronchial mucosa of subjects with chronic bronchitis
Am Rev Respir Dis
(1993) - et al.
CD8+ T-lymphocytes in peripheral airways of smokers with chronic obstructive pulmonary disease
Am J Respir Crit Care Med
(1998) - et al.
Intramural airway inflammation in chronic bronchitis: characterization and correlation with clinical parameters
Am Rev Respir Dis
(1989) - et al.
Differences in interleukin-8 and tumor necrosis factor-α induced sputum from patients with chronic obstructive pulmonary disease or asthma
Am J Respir Crit Care Med
(1996) - et al.
Granulocyte activation markers in induced sputum: comparison between chronic obstructive pulmonary disease, asthma and normal subjects
Am J Respir Crit Care Med
(1997)
Neutrophil elastase and elastase-rich cystic fibrosis sputum degranulate human eosinophils in vitro
Am J Physiol
Effect of smoking cessation on airway inflammation in chronic bronchitis
Am J Respir Crit Care Med
Alveolar inflammation and its relation to emphysema in smokers
Am J Respir Crit Care Med
Inflammatory mediators of asthma; an update
Pharmacol Rev
Lipid mediators in cystic fibrosis and chronic obstructive pulmonary disease
Am Rev Respir Dis
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