Interactions between human respiratory mucins and pathogens.

Three defence mechanisms are responsible for the sterility of the normal tracheobronchial tree: the mucociliary escalator, which continuously traps inhaled micro-organisms; phagocytes; and the bronchial immune system. In the mucociliary system, the respiratory mucus which covers the respiratory mucosa is moved towards the pharnyx as a result of the beating of the cilia covering the airways epithelium, and is swallowed with the trapped bacteria. Mucins are a major macromolecular component of respiratory mucus. They represent a large population of high molecular mass, polydisperse glycoproteins appearing as filaments by electron microscopy [ 1,2]. They are synthesized in goblet cells of the airway surface and in mucous cells of the submucosal glands. They are important in mucus physical organization, and for its rheological properties, which are responsible for the efficiency of the mucociliary escalator. They are also able to interact with various micro-organisms, allowing their elimination from the respiratory tree. The considerable diversity of mucins results from a dual mechanism, a variety of post-translational modifications (glycosylation and sulphation), in addition to the synthesis of various mucin polypeptides or apomucins. Respiratory apomucins (approx. 100-500 kDa) are a family of molecules encoded by different mucin genes, of which at least five genes, MUC2, MUC4, MUCSAC, MUCSB and MUC8, have been identified [3,4].