CC16 levels correlate with cigarette smoke exposure in bronchial epithelial cells and with lung function decline in smokers.

Autor: Lam DC; Department of Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, 21 Sassoon Road, Pokfulam, HK, China. dcllam@hku.hk., Kwok HH; Department of Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, 21 Sassoon Road, Pokfulam, HK, China., Yu WC; Department of Medicine and Geriatrics, Princess Margaret Hospital, Lai King, HK, China., Ko FW; Department of Medicine and Therapeutics, the Chinese University of Hong Kong, Shatin, HK, China., Tam CY; Department of Medicine and Geriatrics, Tuen Mun Hospital, 23, Tsing Chung Koon Rd, Tuen Mun, HK, China., Lau AC; Department of Intensive Care, Pamela Youde Nethersole Hospital, 3, Lok Man Rd, Chai Wan, HK, China., Fong DY; School of Nursing, Li Ka Shing Faculty of Medicine, University of Hong Kong, 21 Sassoon Road, Pokfulam, HK, China., Ip MS; Department of Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, 21 Sassoon Road, Pokfulam, HK, China.
Jazyk: angličtina
Zdroj: BMC pulmonary medicine [BMC Pulm Med] 2018 Mar 16; Vol. 18 (1), pp. 47. Date of Electronic Publication: 2018 Mar 16.
DOI: 10.1186/s12890-018-0607-7
Abstrakt: Background: Club cell protein-16 (CC16) expression has been associated with smoking-related lung function decline. The study hypothesis was that CC16 expression in both serum and bronchial epithelium is associated with lung function decline in smokers, and exposure to cigarette smoke will lead to reduction in CC16 expression in bronchial epithelial cells.
Methods: In a cohort of community-based male Chinese subjects recruited for lung function test in 2000, we reassessed their lung function ten years later and measured serum levels of CC16. CC16 expression was further assayed in bronchial epithelium from endobronchial biopsies taken from an independent cohort of subjects undergoing autofluorescence bronchoscopy, and tested for correlation between CC16 immunostaining intensity and lung function. In an in-vitro model, bronchial epithelial cells were exposed to cigarette smoke extract (CSE), and the expression levels of CC16 were measured in bronchial epithelial cells before and after exposure to CSE.
Results: There was a significant association between FEV 1 decline and serum CC16 levels in smokers. Expression of CC16 in bronchial epithelium showed significant correlation with FEV 1 /FVC. Bronchial epithelial cells showed significant decrease in CC16 expression after exposure to CSE, followed by a subsequent rise in CC16 expression upon removal of CSE.
Conclusions: Results of these clinical and laboratory investigations suggested that low serum CC16 was associated with smoking-related decline in lung function, demonstrated the first time in a Chinese cohort. The data also lend support to the putative role of CC16 in protection against smoking-related bronchial epithelial damage. (Abstract word count: 243) US CLINICAL TRIAL REGISTRY: NCT01185652 , first posted 20 August, 2010.
Databáze: MEDLINE
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