Surfactant protein D is a candidate biomarker for subclinical tobacco smoke-induced lung damage
Author(s) -
Sofie Lock Johansson,
Qihua Tan,
René Holst,
Lene Christiansen,
Niels C. G. Hansen,
Allan Thomas Højland,
Helle Wulf-Johansson,
Anders Schlosser,
Ingrid Louise Titlestad,
Jørgen Vestbo,
Uffe Holmskov,
Kirsten Ohm Kyvik,
Grith Lykke Sørensen
Publication year - 2014
Publication title -
american journal of physiology-lung cellular and molecular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.892
H-Index - 163
eISSN - 1522-1504
pISSN - 1040-0605
DOI - 10.1152/ajplung.00340.2013
Subject(s) - biomarker , pulmonary surfactant , subclinical infection , tobacco smoke , lung , smoke , surfactant protein d , medicine , chemistry , environmental health , biochemistry , organic chemistry , receptor , innate immune system
Variation in surfactant protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage. The association between serum SP-D (sSP-D) and expiratory lung function was assessed in a cross-sectional design in a Danish twin population (n = 1,512, 18-72 yr old). The adjusted heritability estimates for expiratory lung function, associations between SP-D gene (SFTPD) single-nucleotide polymorphisms or haplotypes, and expiratory lung function were assessed using twin study methodology and mixed-effects models. Significant inverse associations were evident between sSP-D and the forced expiratory volume in 1 s and forced vital capacity in the presence of current tobacco smoking but not in nonsmokers. The two SFTPD single-nucleotide polymorphisms, rs1923536 and rs721917, and haplotypes, including these single-nucleotide polymorphisms or rs2243539, were inversely associated with expiratory lung function in interaction with smoking. In conclusion, SP-D is phenotypically and genetically associated with lung function measures in interaction with tobacco smoking. The obtained data suggest sSP-D as a candidate biomarker in risk assessments for subclinical tobacco smoke-induced lung damage. The data and derived conclusion warrant confirmation in a longitudinal population following chronic obstructive pulmonary disease initiation and development.
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