Chronic alcohol intoxication induces hepatic injury through enhanced macrophage inflammatory protein-2 production and intercellular adhesion molecule-1 expression in the liver
Chronic alcohol intoxication induces hepatic injury through enhanced macrophage inflammatory protein-2 production and intercellular adhesion molecule-1 expression in the liver
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DOI：
10.1002/hep.510250214
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发表时间：
1997-02-01
期刊：
影响因子：
13.5
通讯作者：
Bautista, AP
中科院分区：
文献类型：
--
作者：
Bautista, AP
本研究验证了以下假设：长期饮酒直接或间接通过内毒素流入循环，刺激枯否细胞产生巨噬细胞炎性蛋白-2（MIP（2））并上调粘附分子的表达，即，因此，在肝脏中可能发生这些细胞类型之间增强的隔离和细胞-细胞相互作用，这反过来可能导致肝功能改变和肝毒性。在酒精喂养的无特定病原体的雄性Sprague-Dawley大鼠中测试了这一假设。喂养16周后，内毒素（0.2 +/- 0.043 EU/mL）和MIP（2）（625 +/- 100 pg/mL），同时，血清天冬氨酸转氨酶（AST）活性显著升高，肝脏中也观察到少量脂质沉积和炎症样变化，从酒精喂养的大鼠分离的Kupffer细胞在体外释放大量的MIP（2）（>600 pg/10（6）Kupffer细胞/24 hr），与来自成对喂养的大鼠的Kupffer细胞相比，
This study tested the hypothesis that prolonged consumption of alcohol directly or indirectly, through endotoxin influx in the circulation, stimulates the Kupffer cells to produce macrophage inflammatory protein-2 (MIP(2)) and up-regulates the expression of adhesion molecules, i.e., CD18 on PMNs and its counter-receptor, intercellular adhesion molecule-1 (ICAM-1), on hepatic cells, As a result, enhanced sequestration and cell-cell interaction among these cell types may occur in the liver, which in turn could result in altered hepatic function and hepatotoxicity, This hypothesis was tested in alcohol-fed, specific pathogen-free, male Sprague-Dawley rats, After 16 weeks of feeding, endotoxin (0.2 +/- 0.043 EU/mL) and MIP(2) (625 +/- 100 pg/mL) were detected in the sera of alcoholic rats but not in the pair-fed rats, Concomitantly, serum aspartate transaminase (AST) activity was significantly increased, Small lipid deposition and inflammatory-like changes in the liver were also observed, Isolated Kupffer cells from alcohol-fed rats released large amount of MIP(2) (>600 pg/10(6) Kupffer cells/24 hr) in vitro compared with Kupffer cells from pair-fed rats (