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Chemokine involvement in hepatic ischemia/reperfusion injury in mice: Roles for macrophage inflammatory protein‐2 and KC

Chemokine involvement in hepatic ischemia/reperfusion injury in mice: Roles for macrophage... Hepatic injury induced by ischemia and reperfusion is an important clinical problem after liver resection or transplantation. Neutrophils are known to mediate the organ injury, but the precise mechanisms leading to hepatic neutrophil recruitment are undefined. Two CXC chemokines, macrophage inflammatory protein‐2 (MIP‐2) and KC, are potently chemotactic for neutrophils in vitro and have been reported to be involved in neutrophil‐dependent inflammatory tissue injury. The objective of the present study was to determine the roles of MIP‐2 and KC in the induction of hepatic ischemia/reperfusion injury. C57BL/6 mice were subjected to 90 minutes of partial hepatic ischemia followed by reperfusion. Hepatic injury was associated with neutrophil sequestration, edema, and elevated serum levels of hepatic transaminases. The expression of MIP‐2 messenger RNA (mRNA) was induced within 3 hours after reperfusion, before any detectable increase in neutrophil accumulation, and was also increased to a greater extent in the ischemic lobe after 9 hours of reperfusion. These data suggest that MIP‐2 may be involved in the initial recruitment of neutrophils to the ischemic lobe. In contrast, KC mRNA expression was not increased after 3 hours of reperfusion but after 9 hours increased equivalently in both ischemic and non‐ischemic lobes, suggesting a more generalized role in neutrophil recruitment. Neutralization of MIP‐2 or KC resulted in significant decreases in hepatic neutrophil accumulation, edema, and hepatocellular injury. These data suggest that the local expression of MIP‐2 and KC are important mediators involved in neutrophil‐dependent hepatic injury induced by ischemia and reperfusion in mice. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hepatology Wolters Kluwer Health

Chemokine involvement in hepatic ischemia/reperfusion injury in mice: Roles for macrophage inflammatory protein‐2 and KC

Hepatology , Volume 27 (4) – Apr 1, 1998
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Chemokine involvement in hepatic ischemia/reperfusion injury in mice: Roles for macrophage inflammatory protein‐2 and KC

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References (44)

Publisher
Wolters Kluwer Health
Copyright
Copyright © 1998 by the American Association for the Study of Liver Diseases
ISSN
0270-9139
eISSN
1527-3350
DOI
10.1002/hep.510270441
Publisher site
See Article on Publisher Site

Abstract

Hepatic injury induced by ischemia and reperfusion is an important clinical problem after liver resection or transplantation. Neutrophils are known to mediate the organ injury, but the precise mechanisms leading to hepatic neutrophil recruitment are undefined. Two CXC chemokines, macrophage inflammatory protein‐2 (MIP‐2) and KC, are potently chemotactic for neutrophils in vitro and have been reported to be involved in neutrophil‐dependent inflammatory tissue injury. The objective of the present study was to determine the roles of MIP‐2 and KC in the induction of hepatic ischemia/reperfusion injury. C57BL/6 mice were subjected to 90 minutes of partial hepatic ischemia followed by reperfusion. Hepatic injury was associated with neutrophil sequestration, edema, and elevated serum levels of hepatic transaminases. The expression of MIP‐2 messenger RNA (mRNA) was induced within 3 hours after reperfusion, before any detectable increase in neutrophil accumulation, and was also increased to a greater extent in the ischemic lobe after 9 hours of reperfusion. These data suggest that MIP‐2 may be involved in the initial recruitment of neutrophils to the ischemic lobe. In contrast, KC mRNA expression was not increased after 3 hours of reperfusion but after 9 hours increased equivalently in both ischemic and non‐ischemic lobes, suggesting a more generalized role in neutrophil recruitment. Neutralization of MIP‐2 or KC resulted in significant decreases in hepatic neutrophil accumulation, edema, and hepatocellular injury. These data suggest that the local expression of MIP‐2 and KC are important mediators involved in neutrophil‐dependent hepatic injury induced by ischemia and reperfusion in mice.

Journal

Hepatology – Wolters Kluwer Health

Published: Apr 1, 1998

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