Collectively, non-multimerized species of serum SP-D were dominant in COPD and asthmatic patients suggesting that degradation of SP-D takes place to a significant degree in pulmonary disease.
Detection of surfactant proteins A and D (SP-A and SP-D) in the serum of patients with pulmonary diseases is thought to reflect an injury of the alveolar epithelial barrier and as such serve as a biomarker for these diseases.However, the data for SP-B are limited.
Our aim was to examine whether serum surfactant protein D (SP-D) and A (SP-A) could be useful biomarkers of lung damage in obese patients with type 2 diabetes (T2D) without known lung disease.
Our results identify the OSCAR:SP-D interaction as a potential therapeutic target in chronic inflammatory diseases of the lung as well as other diseases involving tissue accumulation of SP-D, infiltration of inflammatory monocytes, and release of TNF-α.
However, we identified no novel surfactant protein D gene (SFTPD) coding or splice region variants in 73 unrelated children with diffuse lung disease from a cohort enriched for genetic surfactant dysfunction.
Serum SP-D in CF patients was increased in parallel with leukocyte count and with reduced FEV-1 and may constitute an alternative biomarker for lung disease, in the clinical setting and in research.
Associations between single nucleotide polymorphisms (SNPs) of the human gene coding surfactant protein-D (SFTPD) and infectious pulmonary diseases have been established by several groups.