Alcohol-induced expression of the CD14 endotoxin receptor protein in rat Kupffer cells

被引：35

作者：

Jarvelainen, HA ^{[1
]}

Oinonen, T ^{[1
]}

Lindros, KO ^{[1
]}

机构：

[1] NATL PUBL HLTH INST,ALCOHOL RES CTR,FIN-00101 HELSINKI,FINLAND

来源：

ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH | 1997年 / 21卷 / 08期

关键词：

endotoxins; alcoholic; liver disease; lipopolysaccharide; CD14; protein;

D O I：

10.1111/j.1530-0277.1997.tb04488.x

中图分类号：

R194 [卫生标准、卫生检查、医药管理];

学科分类号：

摘要：

Gut-derived endotoxins (lipopolysaccharide, LPS) are believed to contribute to alcohol-induced liver disease (ALD) by stimulating Kupffer cells, the resident liver macrophages, to release proinflammatory cytokines. This activation is largely mediated by CD14, a high-affinity membrane-anchored receptor for LPS. We observed, by chemiluminescence-enhanced detection, an increase in immunoreactive CD14 protein in Kupffer cells isolated from rats treated with ethanol for 2 weeks. Immunocytofluorescence experiments confirmed that this increase was confined to the membranes of Kupffer cells from the alcohol-treated rats. The increase was regulated pretranslationally: a 3-fold elevation (p < 0.01) in the hepatic revel of CD14 mRNA was observed. The marked increase in CD14 expression suggests a new mechanism by which alcohol increases the LPS-mediated cytokine signaling by the liver macrophages, thus promoting the interaction between alcohol and endotoxins in the development of liver damage.

引用

页码：1547 / 1551

页数：5

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