Clara cell protein (CC-16) and surfactant-associated protein A (SP-A) in asbestos-exposed workers
(1996) Chest : the cardiopulmonary and critical care journal — Vol. 109, n° 2, p. 467-474 (1996)
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- Abstract
- Asbestos-exposed workers (Asb) can sometimes develop lung impairments resembling idiopathic pulmonary 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 designated CC-10) and surfactant-associated protein A (SP-A). By inhibiting phospholipase A(2) (PLA(2)), CC-16 and SP-A are putative candidates for controlling lung inflammatory events. Both were measured with PLA(2) activity in alveolar fluids (and sera for CC-16) of smoker and nonsmoker Asb and compared with smoking-matched normal subjects (N). CC-16 (in mg/L) was slightly increased in Asb and affected by smoking: nonsmoker Asb: 3.1+/-0.5 vs nonsmoker N: 1.9+/-0.2 (p<0.05), smoker Asb: 1.7+/-0.3 vs smoker N: 0.6+/-0.1 (p<0.05). SP-A (in mu g/mL) was enhanced in Asb but not affected by smoking: 5.4+/-1.5 in Asb vs 1.6+/-0.4 in N (p<0.05), whereas SP-A to phosphorus ratio was increased in Asb but affected by smoking. CC-16 to albumin and CC-16 in serum to alveolar fluid ratios were altered by cigarette consumption in Asb (p<0.05 vs N). Secretory PLA(2) activity was slightly enhanced in Asb (p<0.05 vs N). All data were similar between stages of disease. In summary, alveolar CC-16, SP-A, and secretory PLA(2) activity were increased in Asb. Smoking affected several parameters. By this habit, Asb might reinforce lung profibrotic factors and increase their risk in developing lung alterations resembling IPF.
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Lesur, O., Bernard, AM., & Begin, R. (1996). Clara cell protein (CC-16) and surfactant-associated protein A (SP-A) in asbestos-exposed workers. Chest : the cardiopulmonary and critical care journal, 109(2), 467-474. https://doi.org/10.1378/chest.109.2.467 (Original work published 1996)