Mononuclear cell modulation of fibroblast procoagulant activity.
The release of procoagulant material by connective tissue cells as a sequel to cell injury can initiate blood coagulation and may thus play a role in he pathogenesis of inflammatory lesions. Human foreskin fibroblasts were shown to synthesize high levels of the procoagulant TF in vitro. Generation of TF by fibroblasts was inhibited by addition of supernatants of PHA-stimulated human mononuclear cells to fibroblast cultures. The inhibition was independent of supernatant effects on cellular proliferation and was accompanied by up to a 20-fold increases in PGE2 synthesis in the fibroblast cultures. The inhibition of TF generation by MC-SNs was reversed by adding indomethacin to the fibroblast cultures, suggesting that mononuclear cells suppress fibroblast TF generation by stimulation of endogenous fibroblast synthesis of prostaglandin. Regulation of fibroblast PCA by products of immune cells may be important in the pathogenesis of inflammatory lesions.