The surfactant protein D (SP-D) is produced by type II alveolar cells and se
rves as an antimicrobial agent as well as to prevent inflammation. Our pre
vious study examined single nucleotide polymorphisms in the SP-D gene i
n Taiwanese COPD patients. We found that SP-D gene variants were relate
d to COPD clinical manifestations, severity and prognosis. SP-D levels wer
e significantly associated with COPD airflow obstruction. We found haplot
ype G-G-C-C-A associated with lower COPD risk. COPD patients with hapl
otype G-G-C-C-A had lower serum SP-D levels, higher rates of positive res
ponse to bronchodilator treatment, more improvement of forced expirato
ry volume in 1 s in yearly follow-up and better 3-year survival rate than C
OPD patients with non G-G-C-C-A haplotype. It appears that SP-D haploty
pe can be used as a prognostic factor in Chinese COPD patients. Our invention identifies SP-D gene variants that are predictive of COPD occurrence
and prognosis, and has gained USA patent status. COPD, including chroni
c bronchitis and emphysema, is Taiwan's seventh leading cause of death
and America's third leading cause. Our innovation is that we are the first
team in the world to apply fragment of recombinant human lung surfacta
nt protein D (rfhSP-D) to treat ozone and cigarette-exposed mice model o
f COPD. Exogenous rfhSP-D prevented the formation of oxidized low-den
sity lipoprotein-induced foamy macrophage in vitro and reversed the airw
ay inflammation and emphysematous changes caused by oxidative stress
and CS exposure in vivo. SP-D upregulated the expression of genes involv
ed in countering oxidative stress and lipid metabolism perturbations indu
ced by CS and OxLDL in bone marrow-derived macrophages. We demonst
rate that SP-D plays a crucial role in maintaining the lipid homeostasis of
dysfunctional alveol