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1 Medical Biotechnological Centre, University of Southern Denmark, Odense, Denmark
2 Department of Pathology, Odense University Hospital, Odense, Denmark
3 Department of Biochemistry, University of Oxford, Oxford, United Kingdom
4 Department of Pediatrics, University of California, Davis, CA, USA
5 Copenhagen Blood Transfusion Centre, Copenhagen University Hospital, Denmark
6 Department of Pediatrics and Cardiovascular Research Institute, University of California, San Francisco, CA
7 Department of Cardiology, Aarhus University Hospital (Skejby), Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: uholmskov{at}health.sdu.dk.
Surfactant protein D (SP-D) is an important innate immune defense molecule that mediates clearance of pathogens and modulates the inflammatory response. Moreover, SP-D is involved in lipid homeostasis and pulmonary accumulation of phospholipids has previously been observed in SP-D deficient (Spd-/-) mice. Atherogenesis involves both inflammation and lipid deposition and we investigated the role of SP-D in the development of atherosclerosis. SP-D synthesis was localized to vascular endothelial cells. Atherosclerotic lesion areas were 5.6 fold smaller in the aortic roots in SP-D deficient (Spd-/-) mice compared to wild-type C57BL/6N mice on an atherogenic diet. High-density lipoprotein cholesterol (HDL-C) was significantly elevated the Spd-/- mice. Treatment of the Spd-/- mice, with a recombinant fragment of human SP-D resulted in decreases of HDL-C (21%) as well as total cholesterol (TC) (26%), and low-density lipoprotein (LDL-C) (28%). Plasma tumor necrosis factor-
(TNF-) was reduced in the Spd-/- mice (45% difference). SP-D was proatherogenic in the used mouse model. The effect is likely to be due to the observed disturbances of plasma lipid metabolism and alteration of the inflammatory process, which underlie the reduced susceptibility to atherosclerosis in SP-D deficient mice.
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