Surfactant protein D is a candidate biomarker for subclinical tobacco smoke-induced lung damage

Author:

Johansson Sofie L.1,Tan Qihua23,Holst René4,Christiansen Lene23,Hansen Niels C. G.5,Hojland Allan T.26,Wulf-Johansson Helle1,Schlosser Anders1,Titlestad Ingrid L.5,Vestbo Jørgen5,Holmskov Uffe1,Kyvik Kirsten O.47,Sorensen Grith L.1

Affiliation:

1. Cardiovascular and Renal Research, Institute of Molecular Medicine,

2. The Danish Twin Registry, Epidemiology, Institute of Public Health, and

3. Departments of 4Clinical Genetics and

4. Institute of Regional Health Research, Department of Biostatistics, University of Southern Denmark, Odense;

5. Respiratory Medicine, and

6. Department of Clinical Genetics, Aalborg University Hospital, Aalborg, Denmark

7. Odense Patient Data Explorative Network (OPEN), Odense University Hospital, Odense;

Abstract

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.

Publisher

American Physiological Society

Subject

Cell Biology,Physiology (medical),Pulmonary and Respiratory Medicine,Physiology

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