Repression of CC16 by cigarette smoke (CS) exposure.

Repression of CC16 by cigarette smoke (CS) exposure.
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通过香烟烟雾(CS)暴露对CC16的抑制。

DOI:
10.1371/journal.pone.0116159
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发表时间:
2015
期刊:
影响因子:
3.7
通讯作者:
Chen Y
Chen Y
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Zhu L;Di PY;Wu R;Pinkerton KE;Chen Y

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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.
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