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Differences and similarities between chronic obstructive pulmonary disease and asthma.
Clin Exp Allergy. 1999 Jun; 29 Suppl 2:14-26.CE

Abstract

Asthma and chronic obstructive pulmonary disease (COPD) are complex conditions with imprecise definitions, which make definitive morphological comparisons difficult. The airways in asthma are occluded by tenacious plugs of exudate and mucus, and there is fragility of airway surface epithelium, thickening of the reticular layer beneath the epithelial basal lamina (the last two not usually features of COPD), and bronchial vessel congestion and oedema. There is an increased inflammatory infiltrate comprising 'activated' lymphocytes and eosinophils with release of granular content in the latter, and enlargement of bronchial smooth muscle, particularly in medium-sized bronchi. CD4+ve lymphocytes predominate over CD8+ve cells and neutrophils are sparse. In contrast, three conditions contribute to COPD. In chronic bronchitis there is cough and mucous hypersecretion with enlargement of tracheobronchial submucosal glands and a disproportionate increase of mucous acini. CD8+ve lymphocytes predominate over CD4+ve cells and there are increased numbers of subepithelial macrophages and intra-epithelial neutrophils. Exacerbations of bronchitis are associated with a tissue eosinophilia, apparent absence of IL-5 protein but gene expression for IL-4 and IL-5 is present. In small or peripheral airways disease, there is inflammation of bronchioli and mucous metaplasia and hyperplasia, with increased intraluminal mucus, increased wall muscle, fibrosis, and airway stenoses (also referred to as chronic obstructive bronchiolitis). Respiratory bronchiolitis involving increased numbers of pigmented macrophages is a critically important early lesion. Increasingly severe peribronchiolitis includes infiltration of T lymphocytes in which the CD8+ subset again predominates. These inflammatory changes may predispose to the development of centrilobular emphysema and reduced FEV1 via the destruction of alveolar attachments. In emphysema there is abnormal, permanent enlargement of airspaces distal to the terminal bronchiolus (i.e. within the acinus) accompanied by destruction of alveolar walls and without obvious fibrosis. The severity of emphysema, rather than type, appears to be the most important determinant of chronic deterioration of airflow, and in this there may be significant loss of elastic recoil and microscopic emphysema prior to the observed macroscopic destruction of the acinus.

Authors+Show Affiliations

Imperial College School of Medicine at the National Heart and Lung Institute, London, UK.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

10421818

Citation

Jeffery, P K.. "Differences and Similarities Between Chronic Obstructive Pulmonary Disease and Asthma." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 29 Suppl 2, 1999, pp. 14-26.
Jeffery PK. Differences and similarities between chronic obstructive pulmonary disease and asthma. Clin Exp Allergy. 1999;29 Suppl 2:14-26.
Jeffery, P. K. (1999). Differences and similarities between chronic obstructive pulmonary disease and asthma. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 29 Suppl 2, 14-26.
Jeffery PK. Differences and Similarities Between Chronic Obstructive Pulmonary Disease and Asthma. Clin Exp Allergy. 1999;29 Suppl 2:14-26. PubMed PMID: 10421818.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Differences and similarities between chronic obstructive pulmonary disease and asthma. A1 - Jeffery,P K, PY - 1999/7/28/pubmed PY - 1999/7/28/medline PY - 1999/7/28/entrez SP - 14 EP - 26 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin Exp Allergy VL - 29 Suppl 2 N2 - Asthma and chronic obstructive pulmonary disease (COPD) are complex conditions with imprecise definitions, which make definitive morphological comparisons difficult. The airways in asthma are occluded by tenacious plugs of exudate and mucus, and there is fragility of airway surface epithelium, thickening of the reticular layer beneath the epithelial basal lamina (the last two not usually features of COPD), and bronchial vessel congestion and oedema. There is an increased inflammatory infiltrate comprising 'activated' lymphocytes and eosinophils with release of granular content in the latter, and enlargement of bronchial smooth muscle, particularly in medium-sized bronchi. CD4+ve lymphocytes predominate over CD8+ve cells and neutrophils are sparse. In contrast, three conditions contribute to COPD. In chronic bronchitis there is cough and mucous hypersecretion with enlargement of tracheobronchial submucosal glands and a disproportionate increase of mucous acini. CD8+ve lymphocytes predominate over CD4+ve cells and there are increased numbers of subepithelial macrophages and intra-epithelial neutrophils. Exacerbations of bronchitis are associated with a tissue eosinophilia, apparent absence of IL-5 protein but gene expression for IL-4 and IL-5 is present. In small or peripheral airways disease, there is inflammation of bronchioli and mucous metaplasia and hyperplasia, with increased intraluminal mucus, increased wall muscle, fibrosis, and airway stenoses (also referred to as chronic obstructive bronchiolitis). Respiratory bronchiolitis involving increased numbers of pigmented macrophages is a critically important early lesion. Increasingly severe peribronchiolitis includes infiltration of T lymphocytes in which the CD8+ subset again predominates. These inflammatory changes may predispose to the development of centrilobular emphysema and reduced FEV1 via the destruction of alveolar attachments. In emphysema there is abnormal, permanent enlargement of airspaces distal to the terminal bronchiolus (i.e. within the acinus) accompanied by destruction of alveolar walls and without obvious fibrosis. The severity of emphysema, rather than type, appears to be the most important determinant of chronic deterioration of airflow, and in this there may be significant loss of elastic recoil and microscopic emphysema prior to the observed macroscopic destruction of the acinus. SN - 0954-7894 UR - https://www.unboundmedicine.com/medline/citation/10421818/Differences_and_similarities_between_chronic_obstructive_pulmonary_disease_and_asthma_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0954-7894&date=1999&volume=29&issue=&spage=14 DB - PRIME DP - Unbound Medicine ER -