Mechanisms by which glucocorticosteroids inhibit secretion of mucus in asthmatic airways

A figure is showing a schematic representation of the multifactorial pathogenesis of mucus accumulation in asthmatic airways. This scheme also summarizes many of the known factors participating in increased RGC secretion, and impaired clearance, and suggests at which sites GCS may play a beneficial role. The following points deserve special attention. (1) Mediators released from mast cells, airway cells, and inflammatory cells may all contribute to mucus hypersecretion in the asthmatic. (2) Eicosanoids may have a profound stimulatory effect on mucus secretion. Mast cells and inflammatory cells release factors that cause enhanced production of eicosanoids in the airways. GCS may inhibit the production of these eicosanoids. (3) GCS reduce baseline mucus secretion, perhaps through lipocortin synthesis. (4) Neuronal stimuli increase mucus secretion. (5) Inflammatory cells synthesize a variety of mucus secretagogues. GCS prevent the accumulation of these cells. (6) Other factors, such as gland cell hyperplasia and increased plasma exudation, may all contribute to the increased bronchial secretion. GCS may alter these phenomena. The relative contribution of each of these factors to respiratory hypersecretion is the subject of ongoing research. It is hoped that such research will provide a perspective on which factors are most important and allow for a rational, safe, and effective approach to treating this problem.