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EDITORIAL FOCUS
Medical College of Wisconsin, Children's Research Institute, Milwaukee, Wisconsin
IN THEIR ARTICLE, Snyder et al. (5) provide compelling data that arterial smooth muscle cells of the vessel wall express surfactant protein D (SP-D) and that the expression of SP-D attenuates the release of IL-8 stimulated by LPS and TNF-
. Although most often associated with innate immune protection of the lung, the authors show clearly that arterial smooth muscle cells express SP-D and that SP-D increases the uptake of Chlamydia pneumoniae bodies while attenuating IL-8 expression. These data indicate that SP-D does not abandon its long-standing role in innate immunity simply because it is expressed by a different cell type. Rather, it seems to find ways to help the vasculature rid itself of a foreign antigen, a duty usually relegated to macrophages and dendritic cells.
As IL-8 increases the recruitment of monocytes (4) and neutrophils (3), their data show how vascular smooth muscle cell expression of SP-D may play a role in protecting the vessel wall by attenuating IL-8-mediated inflammation. Thus the findings in their report (5) show for the first time how SP-D protects the vessel wall by a mechanism that has long been recognized to protect the lung. This information could be important in the design of new treatment modalities that increase SP-D expression to decrease vascular inflammation and possibly atherosclerosis.
The exact signaling mechanisms by which SP-D decreases vascular inflammation remain unknown. What is known from the study of Snyder et al. (5), however, is that SP-D blocks both TNF-- and LPS-mediated inflammation. Other studies indicate that SP-D binds to G-P340 (2), signal inhibitory regulatory peptide-, as well as the calreticulin/CD91 complex (1). Accordingly, new opportunities exist for examining a number of promising pathways of activation that could lead to new therapies to block inflammation. Alternatively, SP-D may act by blocking a common mechanism of gene activation such as NF-
B. Thus not only could one design new therapies aimed at increasing vascular SP-D expression to protect the vessel wall, but therapies could be designed to inhibit the pathways targeted by SP-D. Clearly, a continued examination of the role of SP-D in cardiovascular disease should lead to the discovery of new pathways and additional opportunities for inhibiting inflammation in the vessel wall.
FOOTNOTES
Address for reprint requests and other correspondence: K. A. Pritchard, Jr., Medical College of Wisconsin, Children's Research Inst., 8701 Watertown Plank Rd., Milwaukee, WI 53226 (e-mail: kpritch{at}mcw.edu)
REFERENCES
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