Excessive respiratory secretions are a major cause of the airway obstruction in Asthma, Chronic Bronchitis and Cystic Fibrosis. A variety of mediators of immediate hypersensitivity and of acute inflammation have been shown to increase secretion of respiratory mucin glycoprotein. Little data is available on the effect of mediators of inflammation on gene expression of respiratory mucins. The goal of this study is to define the effect of inflammation and of the known mediators of respiratory mucosal inflammation on respiratory mucin gene expression. These studies utilize a respiratory epithelial cell from experimental animals and from a human cell line. Polymerase chain reaction is used to quantitate mucin message utilizing PCR probes designed from previously published mucin gene structure. This data is correlated with secretory studies using an ELISA specific for respiratory mucin.
NIH ExPorter
NIH ExPorter