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As understanding of cellular and molecular mechanisms underlying disease pathogenesis advances, the opportunities increase to identify specific compounds or molecules which are altered by the disease process or appear de novo. These markers of the pathological process have the potential advantage of indices which are indicative of the existing state or change and can be available non-invasively.1
In this issue of Thorax there is a report of the use of Clara cell secretory protein-16 (CC-16, CC-10 or uteroglobulin) as a biomarker for epithelial cell dysfunction (see page 1058).2 CC-16 is a member of the secretoglobin family of secreted disulfide-bridged dimeric proteins.3 It is secreted by non-ciliated Clara cells which reside in respiratory bronchi and by non-ciliated columnar cells of the large and small airways.4 5 CC-16 also occurs in the epithelial cells of the nose and the urogenital tract of men and women.5 There is evidence, however, that serum levels of CC-16 are largely the result of secretion by cells of the respiratory tract rather than the cells of the urogenital tract.6 Serum levels of CC-16 rise following acute exposure to smoke, chlorine and lipopolysaccharide; in patients with asthma, obliterative bronchiolitis and smokers the serum CC-16 levels are low.7 There is an extensive literature on CC-16 levels in serum and bronchoalveolar lavage fluid in normal individuals, experimental animals and individuals exposed to atmospheric pollutants, as well as asthma.7 The exact function of CC-16 is not known, but it may play a role in reducing inflammation in airways.8
The processes which control serum levels of CC-16 are: (1) the rate of synthesis of CC-16 by Clara cells and secretion into the alveolar fluid; (2) the rate of diffusion from alveolar fluid into the capillary blood, which is influenced by leakiness of …
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