Mucus secretion is a normal function of respiratory mucous membranes. Models for measurement of mucus production by cultured human bronchial and nasal mucosae have been developed in order to examine the controls of mucus secretion. In addition to neurohormones and mediators of allergy, airways react to products generated by pulmonary macrophages and peripheral mononuclear cells with increased mucous glycoprotein secretion. The macrophage and mononuclear derived secretagogues are collectively being called macrophage/mononuclear cell derived mucus secretgogues (MMS). Activation of complement leads to anaphylatoxin generation. Current studies indicate that anaphylatoxins may be formed in pulmonary inflammatory processes. Therefore, the effects of human C3a upon mucus release were examined. C3a (and C5a) cause a dose-related stimulation of mucus secretion, maximal at 1-4 hours, apparently not requiring mast cell activation and not reproduced by C3a des arg. Thus, complement derived anaphylatoxins may also participate in mucus secretion. Corticosteroids inhibit MGP release by lowering baseline secretion. Analysis of corticosteroid treated airways reveals a close correlation between lipomodulin generation and MGP production. Pulmonary inflammation with neutrophils is often associated with mucus production. Lysates of human neutrophils as well as supernatants from activated neutrophils causes airways to release MGP; this activity is not due to elastase, and identity of the mucus secretagogue is under study.
