Abstract
Club (Clara) Cell Secretory Protein (CCSP, or CC16) is produced mainly by non-ciliated airway epithelial cells including bronchiolar club cells and the change of its expression has been shown to associate with the progress and severity of Chronic Obstructive Pulmonary Disease (COPD). In an animal model, the lack of CC16 renders the animal susceptible to the tumorigenic effect of a major CS carcinogen. A recent population-based Tucson Epidemiological Study of Airway Obstructive Diseases (TESAOD) has indicated that the low serum CC16 concentration is closely linked with the smoke-related mortality, particularly that driven by the lung cancer. However, the study of CC16 expression in well-defined smoke exposure models has been lacking, and there is no experimental support for the potential causal link between CC16 and CS-induced pathophysiological changes in the lung. In the present study, we have found that airway CC16 expression was significantly repressed in COPD patients, in monkey CS exposure model, and in CS-induced mouse model of COPD. Additionally, the lack of CC16 exacerbated airway inflammation and alveolar loss in the mouse model. Therefore, CC16 may play an important protective role in CS-related diseases.
Highlights
CC16 is a homodimeric protein that was initially attributed to Club cells, but has since been found to be produced by other non-ciliated epithelial cells in the airway [1,2,3,4,5]
Based on the previously reported epidemiological data regarding the reduction of CC16 in serum and lung Broncho alveolar lavage (BAL) in smokers and Chronic Obstructive Pulmonary Disease (COPD) subjects [30,31,32,33,34,35,36], we further looked at the tissuelevel expression of CC16 in diagnosed COPD patients
There was a progressive decrease of epithelial CC16 expression that was correlated with the severity of COPD (Fig. 1D)
Summary
CC16 ( called CC10 or CCSP) is a homodimeric protein that was initially attributed to Club cells (formerly, Clara cells), but has since been found to be produced by other non-ciliated epithelial cells in the airway [1,2,3,4,5]. Besides its abundant presence in the airway lung fluids and sputum, CC16 can be readily detected in the circulation [6,7,8]. CC16 knockout (KO) mice had markedly enhanced inflammation and tissue remodeling in the lung when exposed to a variety. CC16 appears to play an important protective role in inflammatory lung diseases
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