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Laboratory and Animal Investigations |

Clara Cell Secretory Protein*: Levels in BAL Fluid After Smoking Cessation

Olof Andersson, MD, PhD; Tobias N. Cassel, BSc; C. Magnus Sköld, MD, PhD; Anders Eklund, MD, PhD, FCCP; Johan Lund, PhD; Magnus Nord, MD, PhD
Author and Funding Information

*From the Departments of Lung Medicine (Dr. Andersson), Medical Nutrition (Mr. Cassel and Dr. Nord), and Respiratory Medicine (Drs. Sköld and Eklund), Karolinska Institute, Huddinge, Sweden; and the Department of Anatomy and Cell Biology (Dr. Lund), University of Bergen, Norway.

Correspondence to: Olof Andersson, MD, PhD, Department of Lung Medicine, Karolinska Institute, Huddinge University Hospital, Huddinge S-141–86, Sweden; e-mail: olle.andersson@mednut.ki.se



Chest. 2000;118(1):180-182. doi:10.1378/chest.118.1.180
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Study objectives: The bronchiolar Clara cell is a major target for tobacco smoke exposure. To improve our understanding of the putative regenerative/repair mechanism(s) in the bronchiolar epithelium, we measured the levels of the Clara cell secretory protein (CCSP) in BAL fluid in healthy volunteers following smoking cessation.

Design: BAL was performed before smoking cessation, and at 1, 3, 6, 9, and 15 months following smoking cessation, in eight healthy volunteers with a previous mean cigarette consumption of 19 pack-years. The levels of CCSP in BAL fluid were assessed in immunoblotting experiments using an antibody against human CCSP.

Results: Significantly (p < 0.05) higher levels of CCSP in BAL fluid were observed at 3, 6, and 9 months after smoking cessation, while the levels of CCSP in BAL fluid at 15 months after smoking cessation were the same as those before smoking cessation.

Conclusions: Despite the long history of smoking among patients in the present study group, signs of early regeneration in the bronchiolar epithelium were noted, in that the levels of CCSP in BAL fluid were elevated at the indicated time points following smoking cessation. Furthermore, we propose that the insult to the bronchiolar epithelium made by cigarette smoking caused the levels of CCSP in the BAL fluid at 15 months after smoking cessation to return to the levels noted before smoking cessation. The present study suggests a role for CCSP as a marker for nonciliated bronchiolar cell function.

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