Key result
Blocking leukocyte adherence at various levels, such as the beta 2 integrin complex or selectins, may improve outcomes in diseases associated with ischaemia and reperfusion.
Why the study?
Does blocking leukocyte adhesion molecules improve outcomes in ischemia/reperfusion injuries?
Does blocking leukocyte adhesion molecules improve outcomes in ischemia/reperfusion injuries?
Blocking leukocyte adhesion molecules represents a potential therapeutic strategy to reduce ischemia/reperfusion injury.
May support adhesion blockade in ischemia-reperfusion injury; leaves open confirmation in clinical trials.
Tissue ischaemia and/or reperfusion cause some of the injury seen in several clinical disorders and are responsible for considerable mortality and morbidity in humans. Part of the injury occurring after reperfusion of ischaemic tissue is the result of interactions between leukocytes adhering to vascular endothelium. Blocking the function of the leukocyte adhesion beta 2 integrin complex (CD11/CD18) leads to improved outcome following ischaemia and reperfusion. Functional blockade of either P-selectin or L-selectin prevents leukocyte rolling. Blocking leukocyte adherence at one of several levels may provide improved outcome in a variety of diseases associated with ischaemia and reperfusion.
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Winn et al. (2007) conducted a review in Ischaemia/Reperfusion Injuries. Blocking leukocyte adherence (CD11/CD18, P-selectin, L-selectin) was evaluated. Blocking leukocyte adherence at various levels, such as the beta 2 integrin complex or selectins, may improve outcomes in diseases associated with ischaemia and reperfusion.
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