The Role of Cytokines in Pharmacological Modulation of Hepatic Ischemia/Reperfusion Injury
Thomas L. Husted and Alex B. Lentsch
Affiliation: University of Cincinnati,Department of Surgery, 231 Albert Sabin Way, Cincinnati, OH 45267-0558.
Hepatic ischemia/reperfusion injury is a complication of liver resection surgery, transplantation and hypovolemic shock, leading to local and remote cellular damage and organ dysfunction. This injury is largely a result of an acute inflammatory response characterized by the induction of a cascade of proinflammatory mediators that culminates in the recruitment of leukocytes to the post-ischemic tissue leading to parenchymal cell injury. Endogenous regulatory mechanisms exist to attempt to control this inflammatory response. These include anti-inflammatory cytokines that function to suppress proinflammatory mediator expression. In this review, we address the current knowledge of the pro- and anti-inflammatory cytokine components of the acute liver inflammatory response to ischemia/reperfusion as well as how these cytokines can be manipulated to reduce post-ischemic liver injury.
Keywords: Ischemia/reperfusion, inflammation, cytokines, chemokines, adhesion molecules, NF-κB, neutrophils
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