title: Remodeling in asthma and chronic obstructive lung disease.
abstract: Asthma and chronic obstructive lung disease (COPD) are both inflammatory conditions of the lung associated with structural "remodeling" inappropriate to the maintenance of normal lung function. The clinically observed distinctions between asthma and COPD are reflected by differences in the remodeling process, the patterns of inflammatory cells and cytokines, and also the predominant anatomic site at which these alterations occur. In asthma the epithelium appears to be more fragile than that of COPD, the epithelial reticular basement membrane (RBM) is significantly thicker, there is marked enlargement of the mass of bronchial smooth muscle, and emphysema does not occur in the asthmatic nonsmoker. In COPD, there is epithelial mucous metaplasia, airway wall fibrosis, and inflammation associated with loss of surrounding alveolar attachments to the outer wall of small airways: bronchiolar smooth muscle is increased also. Emphysema is a feature of severe COPD: in spite of the destructive process, alveolar wall thickening and focal fibrosis may be detected. The hypertrophy of submucosal mucus-secreting glands is similar in extent in asthma and COPD. The number of bronchial vessels and the area of the wall occupied by them increase in severe corticosteroid-dependent asthma: it is likely that these increases also occur in severe COPD as they do in bronchiectasis. Pulmonary vasculature is remodeled in COPD. In asthma several of these structural alterations begin early in the disease process, even in the child. In COPD the changes begin later in life and the associated inflammatory response differs from that in asthma. The following synopsis defines and compares the key remodeling processes and proposes several hypotheses.
authors.affiliation: Imperial College at the Royal Brompton Hospital, London, United Kingdom. p.jeffery@ic.ac.uk
authors.forename: P K
authors.initials: PK
authors.lastname: Jeffery
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000403:Airway Resistance; D000818:Animals; D001249:Asthma / Q000188:drug therapy / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*; D001485:Basement Membrane / Q000473:pathology / Q000648:ultrastructure; D001706:Biopsy; D001980:Bronchi / Q000473:pathology* / Q000502:physiology / Q000503:physiopathology; D001991:Bronchitis / Q000473:pathology / Q000503:physiopathology; D002648:Child; D002908:Chronic Disease; D004548:Elasticity; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D004848:Epithelium / Q000473:pathology; D000882:Haplorhini; D006801:Humans; D006965:Hyperplasia; D006984:Hypertrophy; D007249:Inflammation / Q000473:pathology; D008168:Lung / Q000473:pathology* / Q000503:physiopathology; D008173:Lung Diseases, Obstructive / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D008855:Microscopy, Electron, Scanning; D009130:Muscle, Smooth / Q000473:pathology / Q000648:ultrastructure; D011650:Pulmonary Alveoli / Q000473:pathology; D011656:Pulmonary Emphysema / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D020545:Respiratory Mucosa / Q000473:pathology; D012907:Smoking / Q000009:adverse effects; D013997:Time Factors