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Bacterial translocation induces procoagulant activity in tissue macrophages. A potential mechanism for end-organ
B J Sullivan1, C J Swallow, M J Girotti
1Department of Surgery, University of Toronto, Ontario, Canada.
Abstract:
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.
Insights
Bacterial translocation, or bacteria moving from the gut, significantly increases cell procoagulant activity in rodents. This suggests a role for bacterial translocation in the development of multiple organ failure.
Area of Science:
- Microbiology
- Pathophysiology
- Immunology
Background:
- Bacterial translocation is a phenomenon where bacteria move from the gastrointestinal tract to normally sterile sites.
- The induction of cell-associated procoagulant activity by bacterial translocation is not well understood.
- Understanding this process may shed light on the pathogenesis of multiple organ failure.
Purpose of the Study:
- To investigate the ability of bacterial translocation to induce cell-associated procoagulant activity in a rodent model.
- To determine the impact of bacterial translocation on procoagulant activity in various cell populations and organs.
Main Methods:
- A rodent model was established using intestinal decontamination and monoassociation with a streptomycin-resistant Escherichia coli strain.
- Bacterial translocation rates were assessed.
- Cell-associated procoagulant activity was measured in mesenteric lymph node mononuclear cells, portal and systemic blood, and hepatic nonparenchymal cells.
Main Results:
- Bacterial translocation rates increased significantly by day 3 in monoassociated animals (90%) compared to controls.
- Procoagulant activity in mesenteric lymph node mononuclear cells was significantly elevated at day 3 in monoassociated animals.
- Hepatic nonparenchymal cell procoagulant activity was also elevated at days 3 and 6 in monoassociated animals.
Conclusions:
- Bacterial translocation can induce cell activation and increase procoagulant activity at sites remote from the gastrointestinal tract.
- These findings suggest that bacterial translocation may contribute to the pathogenesis of multiple organ failure.
- The study highlights the systemic effects of gut bacteria in a controlled experimental setting.