Histopathology of Bronchial Asthma and the Effects of Treatment
Asthma is a complex condition with an imprecise definition. The airways in fatal asthma are occluded by tenacious plugs consisting of a mixture of exudate and mucus. There is fragility of airway surface epithelium and thickening of the subepithelial reticular layer (referred to as the epithelial “basement membrane” by light microscopy). Bronchial vessel dilatation, congestion and oedema, hypertrophy of bronchial smooth muscle and mucus-secreting submucosal glands together with an inflammatory cell infiltrate contribute to thickening of the airway wall. An inflammatory cell infiltrate, comprising lymphocytes and ‘activated’ (EG2+) eosinophils with release of granular content in the latter, are features of fatal asthma and also of relatively mild stable atopic, intrinsic and occupational forms of asthma. Whilst widespread mast cell degranulation (apparent by a reduction in their number) is found in fatal asthma, it is not a feature of mild stable disease as evidenced by studies of the numbers of tryptase positive mast cells and by morphometry of cells examined by electron microscopy. Release of cytokines, particularly IL-5, by lymphocytes, favour selective eosinophil adhesion to endothelium and their differentiation, survival and activation in the mucosa. Short term treatment of atopic asthmatics with inhaled corticosteroid reduces the numbers of mast cells, eosinophils and the extent of eosinophil degranulation. However, neither short-term nor long-term corticosteroid treatment reduces the thickening of reticular basement membrane.
KeywordsCorticosteroid Tuberculosis Polypeptide Histamine Integrin
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