in asbestosis, secrete Clara cell protein (CC-16, also. designatedCC-10)and surfactant-associatedproteinA. (SP-A). Byinhibiting phospholipaseA2 (PLA2), CC- ...
Clara Cell Protein (CC-16) and Surfactant-Associated Protein A (SP-A) in Asbestos-Exposed Workers Olivier Lesur, Alfred M. Bernard and Raymond O. Bégin Chest 1996;109;467-474 DOI 10.1378/chest.109.2.467 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/109/2/467
Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1996by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692
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Clara Cell Protein (CC-16) and Surfactant-Associated Protein A (SP-A) in Asbestos-Exposed Workers* Olivier Lesur, MD, FCCP; Alfred M. Bernard, PhD; and
Raymond O. Begin, MD, FCCP
Asbestos-exposed workers (Asb) can sometimes de¬ idiopathic pulmo¬ velop lung impairments resembling nary fibrosis (IPF). Smoking is often a troubling confounder in the natural history of these lung diseases. Distal airspace epithelial cells, which are also altered in asbestosis, secrete Clara cell protein (CC-16, also A designated CC-10) and surfactant-associated protein (SP-A). By inhibiting phospholipase A2 (PLA2), CC-16 and SP-A are putative candidates for controlling lung with PLA2 inflammatory events. Both were measured for sera in fluids alveolar CC-16) of (and activity smoker and nonsmoker Asb and compared with smoknormal subjects (N). CC-16 (in mg/L) was ing-matched increased in Asb and affected by smoking: slightly nonsmoker Asb: 3.1 ±0.5 vs nonsmoker N: 1.9±0.2 smoker Asb: 1.7±0.3 vs smoker N: 0.6±0.1 (p
