Chest
Volume 117, Issue 5, Supplement 1, May 2000, Pages 251S-260S
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Comparison of the Structural and Inflammatory Features of COPD and Asthma Giles F. Filley Lecture

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At least three conditions contribute to COPD. (1) Chronic bronchitis (mucous hypersecretion) is an inflammatory condition in which CD8+ T-lymphocytes, neutrophils, and CD68+ monocytes/macrophages predominate. The condition is defined clinically by the presence of chronic cough and recurrent increases in bronchial secretions sufficient to cause expectoration. There is enlargement of mucus-secreting glands and goblet cell hyperplasia, which can occur in the absence of airflow limitation. (2) Adult chronic bronchiolitis (small or peripheral airways disease) is an inflammatory condition of small bronchi and bronchioli in which there are predominantly CD8+ and pigmented macrophages. The functional defect is difficult to detect clinically but may be recognized by sophisticated tests of small airway function. There is mucous metaplasia, enlargement of the mass of bronchiolar smooth muscle, and loss of alveolar attachments. (3) Emphysema is an inflammatory condition of the alveoli in which T-lymphocytes, neutrophils, and pigmented alveolar macrophages are involved, associated with the release of excessive amounts of elastases. It is defined anatomically by permanent, destructive enlargement of airspaces distal to terminal bronchioli without obvious fibrosis. In contrast, asthma is a clinical syndrome characterized by allergic inflammation of bronchi and bronchioli in which CD4+ (helper) T-lymphocytes and eosinophils predominate. There is increased production and release of interleukin (IL)-4 and IL-5, which is referred to as a Th2-type response. There is usually increased tracheobronchial responsiveness to a variety of stimuli, and the condition is usually manifest as variable airflow obstruction. While differences between COPD and asthma have been highlighted, new data are emerging that indicate there may also be similarities.

Section snippets

Structural Changes

In bronchial biopsy specimens taken from patients with mild airflow obstruction, there is fragility, damage, and variable loss of surface epithelial cells even in patients with mild stable asthma: the extent of such loss shows a negative correlation with airways hyperresponsiveness2,3,4 (Fig 1, top). Epithelial integrity has not yet been extensively studied in patients with stable chronic bronchitis and COPD, but there are reports of minimal loss.5 In contrast to patients with asthma, the

Structural Changes

The small airway defect in patients with COPD is characterized by persistent airflow limitation, which may show progressive deterioration in the absence of emphysema. While the site of the lesion and its detection in patients with COPD is, as yet, difficult to pinpoint by tests of lung function, experimental physiologists (inter alia42,43) have indicated that the dominant site lies in small bronchi and bronchioli of < 3 mm diameter.

The measurement of sputum only reflects secretions obtained by

Structural Changes

The early changes of emphysema have been thought to include subtle disruption to elastic fibers with an accompanying loss of elastic recoil, bronchiolar and alveolar distortion, and the appearance of fenestrae that enlarge,65,66 an alteration that has been referred to as microscopic emphysema (Fig 8, top and bottom). These biochemical and microscopic changes subsequently lead to the loss, by destruction of the elastic framework, of the interalveolar septa and to the appearance of spaces, > 1 mm

Conclusion and Comment

There is evidence of inflammation in both COPD and asthma, but there are marked differences in terms of the predominant phenotype and the anatomic/mucosal site and in the functional consequences of such inflammation. Inflammation appears to be present throughout the bronchial tree and in the respiratory portion of the lung in patients with COPD. There is inflammation of bronchi and bronchioli in patients with asthma and even eosinophilia of the alveolar/bronchiolar attachment zone. The

ACKNOWLEDGMENTS

I thank Mr. Andrew Rogers for his valuable assistance with the illustrations.

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