Figure 2.

Proposed anti-inflammatory mechanisms for SP-D in the development of atherosclerosis. SP-D plays a dual role in the development of atherosclerosis. This figure aims to depict what we know about the anti-inflammatory properties of SP-D in the development of atherosclerosis. Circulatory SP-D originates from lung-spillover or directly from the atherosclerotic artery. SP-D binds its receptor LAIR-1 on PBMCs, leading to inhibition of ROS and thereby inhibition of the oxidation process of serum LDL. Circulatory SP-D also inhibits circulatory IL-6 and TNF-α and thus the transport of oxidized LDL from the artery lumen to the subendothelial space. SP-D has been shown to inhibit the proliferation of Th1 cells and their secretion of IFN-γ and TNF-α; this ultimately leads to inhibition of activated macrophages and foam cell formation. TNF-α secretion from NK cells and foam cells stimulates vascular smooth muscle cells (VSMC) to produce and secrete SP-D into the subendothelial space, where it again exerts its negative-feedback loop on NK cells. SP-D is able to inhibit IL-8 from LPS-stimulated VSMC, thus decreasing vascular inflammation.