Pathological Features of Asthma

Asthma is characterized by variable damage to the bronchial epithelium and increased numbers of airway mucosal and submucosal inflammatory cells, including eosinophils, mast cells, and T lymphocytes (19-21). Other prominent features of asthma include hypertrophy and hyperplasia of airway smooth muscle, basement membrane thickening, mucosal edema and excessive secretion of mucus, all of which contribute to airway narrowing (22). 

In severe exacerbations both large and small airways show gross damage and shedding of the epithelium, and the airways may become occluded by inspissated mucus and cellular debris, which form tenacious plugs (Fig. 1). Studies 

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Figure 1 Characteristic pathological features of asthma (a) Epithehal disruption, suh-basement membrane collagen deposition and infiltration of the submucosa with inflammatory cells—specifically eosinophils, mast cells, T cells, and tissue macrophages (b) Epithelial metaplasia with an increase in goblet cells. Chronic asthma is also characterized by hyperplasia of airway smooth muscle beneath the inflamed submucosa and the deposition of matrix proteins both in the submucosa and adventitia of the airway (H E stain).

Over a decade of research and clinical efforts in the immunopathogenesis of asthma (1,2) have substantiated the critical role of airway inflammation and identified key mediators and mechanisms. Because information on the pathological features of asthma was first obtained from postmortem examination of severe asthmatics, airway inflammation was believed to be a feature of advanced, terminal disease (3). Those airways showed infiltration by granulocytes (neutrophils, eosinophils), increased numbers of lymphocytes, activated mast cells, collagen deposition beneath the basement membrane, and occlusion of the bronchial lumen by mucus produced from hyperplastic goblet cells. The finding of hypertrophied bronchial smooth muscle supported the widely held belief that asthma was primarily a disease of airway smooth muscle. 

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