THE PATHOBIOLOGY OF BRONCHIAL-ASTHMA

This chapter discusses the recent developments in research on the pathobiology of the disease. The focus is on the cellular mechanisms of the disease as indicated by current information on the pathologic changes in the asthmatic bronchial mucosa obtained in living patients via the fiberoptic bronchoscope. The mediator mechanisms are addressed with special consideration of the possible role of the sulfidopeptide leukotrienes, prostanoid metabolites, and platelet-activating factor. Bronchial asthma is not a homogeneous disease and there are well-defined subgroups of patients. Heterogeneity in asthmatic syndromes is addressed by a consideration of two well-defined clinical subgroups—namely, aspirin-induced asthma and corticosteroid-resistant bronchial asthma. Bronchial asthma is a disease that is characterized by a history of episodic wheezing, by physiologic evidence of reversible airflow obstruction, either spontaneously or following bronchodilator therapy, and by pathologic evidence of inflammatory changes in the bronchial mucosa. Subsequent histological studies of the airways and examination of bronchoalveolar lavage fluid of subjects with mild asthma have confirmed the presence of airway inflammation in life. There is epithelial edema and desquamation, subepithelial deposition of collagen and fibronectin, and an inflammatory cell infiltrate in the mucosa. © 1992 Academic Press Inc.