[Interaction between neutrophils and endothelial cells following ischemia/reperfusion].
The adherence of activated neutrophils to endothelial cells during ischemia/reperfusion injury is mediated by inside-out signal transduction. Subsequently, outside-in signal transduction occurs following ligation of adhesion molecules with their ligands triggering respiratory bursts of neutrophils. In addition, neutrophil elastase enhances CC- and CXC-chemokine production by monocytes and macrophages. MCP-1, a CC-chemokine, enhances tissue factor production by macrophages and increases ICAM-1 expression on endothelial cells. Chemotaxis and respiratory bursts of neutrophils are augmented by CXC-chemokines. Furthermore, neutrophil elastase inactivates anticoagulants including antithrombin III, heparin cofactor II, and thrombomodulin, suggesting that neutrophil elastase aggravates microcirculatory disturbance after ischemia/reperfusion. Thus neutrophil elastase modulates the interation of neutrophils and endothelial cells during ischemia/reperfusion injury. Taken together with these observations, a therapeutic regimen with antibodies against adhesion molecules in combination with neutrophil elastase inhibitor and anticoagulants may attenuate ischemia/reperfusion injury.
Department of Surgery II, Kumamoto University Medical School, Japan.
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Yamaguchi
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Ogawa
D000818:Animals; D002448:Cell Adhesion / Q000502:physiology; D002450:Cell Communication; D004730:Endothelium, Vascular / Q000166:cytology*; D009504:Neutrophils / Q000502:physiology*; D051381:Rats; D015427:Reperfusion Injury / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology