Effects of interleukin-1, lipopolysaccharide, and streptococci on procoagulant activity of cultured human cardiac valve endothelial and stromal cells

Abstract

Fibrin is the primary constituent of the vegetation in infective endocarditis, and tissue factor expression is a major mechanism of coagulation activation on infected valves. To determine which cells may participate in coagulation activation in this setting, expression of procoagulant activity (PCA; shown to be tissue factor) was studied in cultured endothelial and stromal cells derived from human cardiac valves. Endothelial cells had negligible PCA (99 ± 50 mU/105 cells, mean ±1 standard deviation) unless stimulated by lipopolysaccharide or interleukin-1, which increased PCA to 5,592 ± 1,482 and 5,901 ± 1,497 mU/105 cells, respectively, in 6 h. Incubation of cells with viable enterococci or viridans streptococci or with an enterococcal cell wall preparation did not induce PCA. Cultured valve stromal cells constitutively expressed high levels of PCA (14,276 ± 8,738 mU/105 cells) which was not changed with exposure to interleukin-1. PCAs of stromal or stimulated endothelial cells from valves of both right and left sides of the heart were comparable. The results suggest that endothelial cells may contribute to fibrin deposition during infection if stimulated, but PCA is not directly induced by bacteria. Stromal cells could contribute PCA if exposed to blood in the course of valve injury.