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Clinically applicable thermal preconditioning attenuates leukocyte-endothelial interactions.
Paul H McCormick1, Gang Chen, Sean Tierney
1Department of Surgery, Royal College of Surgeons of Ireland, Beaumont Hospital, Dublin, Ireland.
Journal of the American College of Surgeons
|July 2, 2003
Summary
Clinically applicable thermal preconditioning reduces ischemia-reperfusion (I/R) injury by attenuating leukocyte-endothelial interactions. This protective effect is linked to increased heat shock protein 72 (HSP72) expression.
Area of Science:
- Physiology
- Immunology
- Cell Biology
Background:
- Ischemia-reperfusion (I/R) injury involves leukocyte-endothelial cell interactions.
- Clinically applicable thermal preconditioning induces heat shock protein 72 (HSP72).
- HSP72 protects against I/R injury.
Purpose of the Study:
- To investigate if thermal preconditioning's protective effects against I/R injury are mediated by attenuating leukocyte-endothelial (L-E) interactions.
- To explore the role of HSP72 in this process.
Main Methods:
- Thermal preconditioning applied to Sprague Dawley rats for 5 days.
- I/R injury induced via superior mesenteric artery occlusion.
- Leukocyte-endothelial interactions analyzed using intravital microscopy.
- Leukocyte velocity, adhesion, and migration quantified.
- HSP72 expression assessed via Western blot.
Main Results:
- I/R significantly decreased leukocyte rolling velocity and increased adhesion/migration.
- Thermal preconditioning significantly improved leukocyte rolling velocity post-I/R.
- Preconditioning attenuated leukocyte adhesion and migration to control levels.
- Upregulation of HSP72 was confirmed.
Conclusions:
- Clinically applicable thermal preconditioning offers protection against I/R injury.
- This protection is partly due to an immunomodulatory role in attenuating L-E interactions.
- Increased HSP72 expression is associated with these beneficial effects.
