title: Mucin-producing elements and inflammatory cells.
abstract: Airway goblet cells and submucosal glands form the major sources of human respiratory mucins. In the adult, mucus-secreting glands occupy about one-third of the inner airway wall wherever there is supportive cartilage (i.e. from the larynx to small bronchi). In hypersecretory conditions such as chronic bronchitis, asthma and cystic fibrosis, glands are considered to be the major source of tracheobronchial mucus, especially that which is expectorated abnormally as sputum. In contrast, goblet cells are regularly found throughout the tracheobronchial tree. Normally sparse or absent in bronchioles (i.e. small airways of less than 1 mm diameter), goblet cells appear and increase in number in airway hypersecretory conditions: their secretions likely contribute to airflow obstruction and early closure of bronchioles, especially during expiration. The increase in gland mass has been considered to be the histological correlate of mucus-hypersecretion in conditions such as chronic bronchitis. However, there appears to be a better association of sputum production with scores of airway wall inflammation than with gland size per se. Thus, while the absolute mass of mucus-secreting tissue is important, it is likely that the release of inflammatory cell secretions (e.g. neutrophil elastase, mast cell chymotryptase), mediators of inflammation (e.g. interleukin 4, 13) and products of the metabolism of arachidonic acid (such as 15-HETE) contribute more than previously realized to the hypersecretion of mucus in chronic bronchitis. New data discussed herein provide supportive evidence for this hypothesis and identify a newly reported link between plasma cells and mucus-hypersecretion by submucosal glands. These considerations demonstrate the complexity of targets that need to be considered for the treatment of mucus hypersecretion.
authors.affiliation: Lung Pathology, Department of Gene Therapy, Imperial College School of Medicine, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK.
authors.forename: Peter
authors.initials: P
authors.lastname: Jeffery
authors.forename: Jie
authors.initials: J
authors.lastname: Zhu
mesh_terms: D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D001991:Bronchitis / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000502:physiology; D004802:Eosinophilia / Q000378:metabolism / Q000473:pathology; D005088:Exocrine Glands / Q000378:metabolism* / Q000473:pathology; D005089:Exocytosis; D020397:Goblet Cells / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D006984:Hypertrophy; D016131:Lymphocyte Subsets / Q000378:metabolism; D008407:Mast Cells / Q000502:physiology; D008954:Models, Biological; D009077:Mucins / Q000096:biosynthesis*; D009093:Mucus / Q000378:metabolism*; D009504:Neutrophils / Q000502:physiology; D018384:Oxidative Stress; D010950:Plasma Cells / Q000276:immunology; D051381:Rats; D012141:Respiratory Tract Infections / Q000276:immunology; D012636:Secretory Rate; D012907:Smoking / Q000503:physiopathology; D014136:Tracheitis / Q000378:metabolism / Q000473:pathology*
chemical_list: D001095:Arachidonic Acids; D016207:Cytokines; D009077:Mucins