Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 294, Issue 5, Pages H2053-H2059Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.91529.2007
Keywords
inflammation; Chlamydia pneumoniae; innate immunity; interleukin-8
Funding
- NHLBI NIH HHS [R01 HL070860, R01 HL076684, 2T32 HL 07638-16, HL 076684, HL 070860, R01 HL050050, P01 HL062984, HL 50050, T32 HL007638, HL 62984, R01 HL070860-02] Funding Source: Medline
- NIDDK NIH HHS [DK 25295] Funding Source: Medline
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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-alpha-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-alpha 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.
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