Key result
Platelet activating factor amplified lipopolysaccharide-induced tissue factor activity in monocytes by 80% in whole blood, requiring the presence of both platelets and granulocytes.
PAF enhances LPS-induced tissue factor activity in monocytes through a mechanism requiring both platelets and granulocytes.
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Animal data on PAF-monocyte interactions do not change practice; leaves open mechanistic role in human thrombosis.
Incubation of platelet activating factor (PAF) with heparinized blood caused no induction of tissue factor activity in monocytes. However, when PAF was added in addition to weak lipopolysaccharide (LPS), it amplified the LPS effect by 80%. By using separated fresh cell populations resuspended in plasma, PAF was shown to have no enhancing effect when added to mononuclear cells incubated with platelet-rich plasma in the presence of LPS. In contrast, when granulocytes also were included, PAF caused an almost 3-fold increase in LPS-induced tissue factor activity. A PAF antagonist blocked this effect and also reduced LPS-induced tissue factor activity of monocytes in whole blood in a dose-dependent manner. In the recombined cell incubation system, the maximal inhibition by the antagonist was observed in the presence of granulocytes. These data provide evidence for an effect of PAF on granulocytes that probably generates a product that, together with platelets, enhances LPS-induced tissue factor activity in monocytes.
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Bjarne Østerud (1992) studied this question. Platelet activating factor (PAF) vs. Lipopolysaccharide (LPS) alone was evaluated on LPS-induced tissue factor activity in monocytes (80% amplification). Platelet activating factor amplified lipopolysaccharide-induced tissue factor activity in monocytes by 80% in whole blood, requiring the presence of both platelets and granulocytes.
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