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Surfactant protein D is expressed and modulates inflammatory responses in human coronary artery smooth muscle cells

Departments of ¹Internal Medicine, ²Anatomy and Cell Biology, and ³Emergency Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa; and ⁴Department of Internal Medicine, University of Cincinnati College of Medicine, and ⁵Veteran's Administration Medical Center, Cincinnati, Ohio

Submitted 27 December 2007 ; accepted in final form 13 March 2008

Surfactant protein D (SP-D) is a constituent of the innate immune system that plays a role in the host defense against lung pathogens and in modulating inflammatory responses. While SP-D has been detected in extrapulmonary tissues, little is known about its expression and function in the vasculature. Immunostaining of human coronary artery tissue sections demonstrated immunoreactive SP-D protein in smooth muscle cells (SMCs) and endothelial cells. SP-D was also detected in isolated human coronary artery SMCs (HCASMCs) by PCR and immunoblot analysis. Treatment of HCASMCs with endotoxin (LPS) stimulated the release of IL-8, a proinflammatory cytokine. This release was inhibited >70% by recombinant SP-D. Overexpression of SP-D by adenoviral-mediated gene transfer in HCASMCs inhibited both LPS- and TNF--induced IL-8 release. Overexpression of SP-D also enhanced uptake of Chlamydia pneumoniae elementary bodies into HCASMCs while attenuating IL-8 production induced by bacterial exposure. Both LPS and TNF- increased SP-D mRNA levels by five- to eightfold in HCASMCs, suggesting that inflammatory mediators upregulate the expression of SP-D. In conclusion, SP-D is expressed in human coronary arteries and functions as an anti-inflammatory protein in HCASMCs. SP-D may also participate in the host defense against pathogens that invade the vascular wall.

inflammation; Chlamydia pneumoniae; innate immunity; interleukin-8

This article has been cited by other articles:

				K. A. Pritchard Jr. Surfactant protein D: not just for the lung anymore Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H1994 - H1994. [Full Text] [PDF]