Decreasing the expression of LFA-1 and ICAM-1 as the major mechanism for the protective effect of hyperbaric oxygen on ischemia-reperfusion injury
✍ Scribed by Hamid Namazi
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 35 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0738-1085
No coin nor oath required. For personal study only.
✦ Synopsis
This work shows that hyperbaric oxygen markedly suppresses neutrophil infiltration compared with a placebo. I would like to complete the discussion of Vidigal et al. 1 by introducing a major route through which hyperbaric oxygen could suppress the activity of neutrophils.
Ischemia-reperfusion injury is a common surgical event in orthopedics, with tourniquet use being a recognized cause. Reperfusion of the acutely injured limb is a commonly occurring event associated with local and systemic proinflammatory responses, which may account for significant morbidity and mortality. 2,3 Transendothelial migration of neutrophils, with release of reactive oxygen species and cytokines, causes further damage to the injured tissue. 4 However, a key component in the pathogenesis of reperfusion syndrome is the upregulation of surface adhesion molecules on the vascular endothelium and their subsequent interaction with the activated neutrophils. The most important adhesion protein identified on neutrophils is the integrin lymphocyte function-associated antigen-1 (LFA-1; CD11a/CD18), which is the ligand for intercellular adhesion molecule-1 (ICAM-1) expressed on the endothelium. The LFA-1/ICAM-1 interaction is crucial for the ingress of neutrophils into the inflammatory sites. 5,6 Hyperbaric oxygen downregulate the expression of ICAM-1 and LFA-1, and through binding to LFA-1, they interfere with ICAM-1-LFA-1 interaction. 7,8 This important mechanism should be borne in mind as the major mechanism for hyperbaric oxygen-induced inhibition of neutrophil activity.