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Am J Physiol Heart Circ Physiol 290: H2286-H2294, 2006. First published December 30, 2005; doi:10.1152/ajpheart.01105.2005
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Surfactant protein D is proatherogenic in mice

Grith L. Sorensen,1 Jens Madsen,1 Karin Kejling,1 Ida Tornoe,1 Ole Nielsen,2 Paul Townsend,3 Francis Poulain,4 Claus H. Nielsen,5 Kenneth B. M. Reid,3 Samuel Hawgood,6 Erling Falk,7 and Uffe Holmskov1

1Medical Biotechnological Center, University of Southern Denmark, and 2Department of Pathology, Odense University Hospital, Odense, Denmark; 3Department of Biochemistry, Medical Research Council Immunochemistry Unit, University of Oxford, Oxford, United Kingdom; 4Department of Pediatrics, University of California, Davis, California; 5Copenhagen Blood Transfusion Centre, Copenhagen University Hospital, Copenhagen, Denmark; 6Department of Pediatrics and Cardiovascular Research Institute, University of California, San Francisco, California; and 7Department of Cardiology, Aarhus University Hospital (Skejby), Aarhus, Denmark

Submitted 19 October 2005 ; accepted in final form 23 December 2005

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 Spd–/– mice compared with wild-type C57BL/6N mice on an atherogenic diet. HDL cholesterol (HDL-C) was significantly elevated in Spd–/– mice. Treatment of Spd–/– mice with a recombinant fragment of human SP-D resulted in decreases of HDL-C (21%) as well as total cholesterol (26%), and LDL cholesterol (28%). Plasma TNF-{alpha} was reduced in Spd–/– mice (45% difference). SP-D was proatherogenic in the mouse model used. 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 Spd–/– mice.

atherosclerosis; experimental animals; high-density lipoprotein; tumor necrosis factor-{alpha}


Address for reprint requests and other correspondence: U. Holmskov, Univ. of Southern Denmark, Medical Biotechnology Center, Winsloewparken 25,3, 5000 Odense C, Denmark (e-mail: uholmskov{at}health.sdu.dk)




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