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Isolation and Characterization of Neutrophils with Anti-Tumor Properties
Published on: June 19, 2015
Effect of hyperbaric oxygen on neutrophil CD18 expression
J L Larson1, L L Stephenson, W A Zamboni
1Division of Plastic Surgery, University of Nevada School of Medicine, Las Vegas 89102-2227, USA.
Plastic and Reconstructive Surgery
|April 1, 2000
Summary
Hyperbaric oxygen did not reduce neutrophil CD18 adhesion sites in a rat ischemia-reperfusion injury model. Ischemia-reperfusion increased CD18 expression, but hyperbaric oxygen did not alter this effect.
Area of Science:
- Biomedical Engineering
- Physiology
- Immunology
Background:
- Neutrophil adhesion is a key factor in ischemia-reperfusion injury.
- Hyperbaric oxygen therapy (HBOT) has shown potential in reducing this adhesion.
- The precise mechanism by which HBOT affects neutrophil adhesion remains unclear.
Purpose of the Study:
- To investigate the effect of hyperbaric oxygen on neutrophil CD18 adhesion site expression.
- To elucidate the mechanism of HBOT's action in a rat model of ischemia-reperfusion injury.
Main Methods:
- A rat model of gracilis muscle ischemia-reperfusion injury was established.
- Three groups were studied: sham, ischemia-reperfusion, and ischemia-reperfusion with HBOT.
- Neutrophil CD18 expression was quantified using flow cytometry and antibody binding capacity.
Main Results:
- Ischemia-reperfusion injury significantly increased neutrophil CD18 expression.
- Hyperbaric oxygen treatment did not decrease the elevated CD18 expression.
- Phorbol-12 myristate 13-acetate stimulation universally increased CD18 expression across all groups.
Conclusions:
- Ischemia-reperfusion injury elevates neutrophil CD18 expression.
- Hyperbaric oxygen, under the conditions tested, does not mitigate this increase in CD18 expression.
- The mechanism of HBOT's previously observed reduction in neutrophil adhesion may not involve direct modulation of CD18 expression sites.
