Bacterial translocation induces procoagulant activity in tissue macrophages. A potential mechanism for end-organ dysfunction.

The ability of bacterial translocation to induce cell-associated procoagulant activity was examined in a rodent model. Intestinal decontamination with streptomycin sulfate and bacitracin followed by oral feeding with a streptomycin-resistant strain of Escherichia coli produced monoassociation of the gastrointestinal tract with this microorganism. Using this model, the rate of bacterial translocation at day 3 increased from 6% (1 of 17) to 90% (28 of 31). Cell-associated procoagulant activity was measured in the mononuclear cell population of mesenteric lymph nodes as well as portal and systemic blood and also in hepatic nonparenchymal cells. In monoassociated animals, the procoagulant activity of mesenteric lymph node mononuclear cells was significantly greater than in control animals at day 3 (210% +/- 28% vs 100% +/- 6%) but not at days 1 or 6. Procoagulant activity of hepatic nonparenchymal cells was elevated in monoassociated animals at days 3 and 6 compared with control animals. Both control and monoassociated animals remained well throughout the experiment. The histologic features of the gastrointestinal tract, mesenteric nodes, and liver did not differ between groups. These studies provide evidence that bacterial translocation, in the absence of external stimuli, is able to induce cell activation at sites remote from the gastrointestinal tract and may therefore contribute to the pathogenesis of multiple organ failure.