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Comprehensive characterisation of pulmonary and serum surfactant protein D in COPD

: Winkler, C.; Atochina-Vasserman, E.N.; Holz, O.; Beers, M.F.; Erpenbeck, V.J.; Krug, N.; Roepcke, S.; Lauer, G.; Elmlinger, M.; Hohlfeld, J.M.

Postprint urn:nbn:de:0011-n-1571728 (904 KByte PDF)
MD5 Fingerprint: 4b1fdbca1cf3694d28ded1f27cd02bcb
Created on: 7.4.2011

Respiratory research. Online journal 12 (2011), Art. 29, 11 pp.
ISSN: 1465-993X
ISSN: 1465-9921
Journal Article, Electronic Publication
Fraunhofer ITEM ()

BACKGROUND: Pulmonary surfactant protein D (SP-D) is considered as a candidate biomarker for the functional integrity of the lung and for disease progression, which can be detected in serum. The origin of SP-D in serum and how serum concentrations are related to pulmonary concentrations under inflammatory conditions is still unclear.
METHODS: In a cross-sectional study comprising non-smokers (n = 10), young - (n = 10), elderly smokers (n = 20), and smokers with COPD (n = 20) we simultaneously analysed pulmonary and serum SP-D levels with regard to pulmonary function, exercise, repeatability and its quaternary structure by native gel electrophoresis. Statistical comparisons were conducted by ANOVA and post-hoc testing for multiple comparisons; repeatability was assessed by Bland-Altman analysis.
RESULTS: In COPD, median (IQR) pulmonary SP-D levels were lower (129(68) ng/ml) compared to smokers (young: 299(190), elderly: 296(158) ng/ml; p < 0.01) and non-smokers (967(708) ng/ml; p < 0.001). The opposite was observed in serum, with higher concentrations in COPD (140(89) ng/ml) as compared to non-smokers (76(47) ng/ml; p < 0.01). SP-D levels were reproducible and correlated with the degree of airway obstruction in all smokers. In addition, smoking lead to disruption of the quaternary structure.
CONCLUSIONS: Pulmonary and serum SP-D levels are stable markers influenced by smoking and related to airflow obstruction and disease state. Smaller subunits of pulmonary SP-D and the rapid increase of serum SP-D levels in COPD due to exercise support the translocation hypothesis and its use as a COPD biomarker.
TRIAL REGISTRATION: no interventional trial.