L-selectin and chemokine response after liver ischemia and reperfusion
L-selectin and chemokine response after liver ischemia and reperfusion
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DOI:
10.1006/jsre.2000.5954
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发表时间:
2000-09-01
影响因子:
2.2
通讯作者:
Ward, PA
中科院分区:
文献类型:
--
作者:
Martinez-Mier, G;Toledo-Pereyra, LH;Ward, PA
Background L-selectin plays an important role in the early phase of PMNs recruitment in the hepatic microvasculature following liver ischemia and reperfusion (I/R). Leukocyte cytokine chemoattractants (chemokines) cause polymorphonuclear neutrophil (PMN) activation in I/R injury. In this study, me examined the role of L-selectin in the production of chemokines in the Liver and lung inflammatory response following 90 min of warm ischemia,Study design. Thirty-six C57BL/6 mice were subjected to partial liver ischemia for a period of 90 min. Three groups of animals were included (n = 12 per group)-sham group, ischemic control, and the ischemic group receiving monoclonal antibody against L-selectin. We evaluated at 3 h: liver injury measurements, serum chemokines (MIP-2 and MIP-1 alpha), liver and lung tissue myeloperoxidase (MPO), and liver and lung histology. statistical analysis included ANOVA, Student-Newman-Keuls', and Kruskal-Wallis multiple comparison Z-value tests.Results. The ischemic group treated with anti-L-selectin showed significant decreases in liver enzyme levels and a marked decrease in serum MIP-2 (P < 0.05) when compared to ischemic controls. No reduction in serum MIP-1 alpha was noted; however, neutrophil infiltration was significantly ameliorated in the liver and in the lung, as reflected by decreased MPO levels (P < 0.05). Improved histopathological features were observed in the anti-L-selectin-treated group compared to ischemic controls in the Liver and the lung.Conclusions. Our study suggests an important role for L-selectin in the pathogenesis of Liver I/R and the production of chemokines. Anti-L-selectin treatment resulted in improved liver function, decreased neutrophil infiltration, and decreased MIP-2 chemokine response. (C) 2000 Academic Press.