Remodeling and inflammation of bronchi in asthma and chronic obstructive pulmonary disease

Abstract

Asthma and chronic obstructive pulmonary disease (COPD) are pathologically distinct in terms of their predominant inflammatory cells and structural alterations (i.e., remodeling). However, there are many cases of functional and pathologic overlap, supporting the author's view that use of the terms asthma or COPD is oversimplistic and fails to identify the range of phenotypes that exist. In general, there is epithelial fragility and thickening of the reticular basement membrane, even in mild asthma; increased airway smooth muscle mass, hypertrophy of mucus-secreting glands, increased vascularity, greater numbers of fibroblasts, and increased deposition of collagen in severe asthma and COPD; and mucous metaplasia, squamous metaplasia, and parenchymal destruction in COPD. Because of increased neutrophilia, patterns of inflammation become similar when exacerbations of asthma and COPD result in hospitalization. Moreover, in mild COPD, exacerbations of bronchitis are associated with mucosal eosinophilia and upregulation of RANTES, two features normally associated with asthma. The overlap may also be seen in intermediate thickening of the reticular basement membrane and eosinophilia in patients with COPD who demonstrate reversibility to oral steroid. Importantly, a recent study of "eosinophilic bronchitis" demonstrates a thickened reticular basement membrane and challenges our current concept of the histopathologic distinctions between asthma and COPD.