The respiratory tract is continuously exposed to foreign antigens and potential pathogenic microorganisms. The tracheobronchial mucosa must interact with these substances and, in certain chronic inflammatory states such as asthma, may participate in the pathogenesis of disease. The mechanisms that regulate normal and abnormal inflammatory responses in the upper respiratory tract are poorly understood. Whole tissue studies suggest that respiratory epithelium produces factor (s) that can modulate inflammatory cell activity (1). Studies of highly enriched epithelial cell cultures devoid of resident immune cells indicate that airway epithelial cells produce arachidonic acid metabolites (2, 3). Epithelial cells of the upper airway also express major histocompatibility