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Published on: June 29, 2015
Antithrombin modulates the leukocyte-endothelial cell interaction in the staphylococcal enterotoxin B-challenged
Toshiaki Iba1, Akio Kidokoro, M Fukunaga
1Department of Surgery, Juntendo University Urayasu Hospital, Juntendo University, School of Medicine, Tomioka, Japan. iba-jun@umin.ac.jp
Antithrombin protects against supertoxin-induced sepsis by reducing leukocyte-endothelial cell interactions. This treatment also suppressed inflammatory markers, offering a potential therapeutic strategy for sepsis.
Area of Science:
- Sepsis research
- Microcirculation studies
- Inflammatory mediator analysis
Background:
- Antithrombin is known for its beneficial effects in endotoxemia.
- This study investigates antithrombin's role in supertoxin-induced sepsis.
Purpose of the Study:
- To evaluate the protective effects of antithrombin in a mouse model of sepsis induced by staphylococcal enterotoxin B.
- To analyze the impact of antithrombin on microcirculation and humoral mediators during sepsis.
Main Methods:
- Mice were administered staphylococcal enterotoxin B and antithrombin concurrently.
- Mesenteric microcirculation was assessed using intravital microscopy 1 hour post-injection.
- Humoral mediators, including adhesion molecules and cytokines, were quantified.
Main Results:
- Antithrombin significantly reduced rolling leukocyte-endothelial cell interactions (p < 0.01).
- The decrease in white blood cell and platelet counts was significantly inhibited in antithrombin-treated mice (p < 0.01).
- Elevated levels of intercellular adhesion molecule-1 (p < 0.05), soluble tumor necrosis factor-alpha receptor (p < 0.05), and interleukin-6 (p < 0.01) were attenuated.
Conclusions:
- Antithrombin demonstrates protective effects on microcirculation in a staphylococcal enterotoxin B-induced sepsis model.
- The mechanism involves attenuating leukocyte-endothelial cell interactions.
- Suppression of adhesion molecule expression and cytokine production contributes to antithrombin's protective role.
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