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Comparative Analysis of Hepatic CD14 Expression between Two Different Endotoxin Shock Model Mice: Relation between Hepatic Injury and CD14 Expression

机译:两种内毒素休克模型小鼠肝CD14表达的比较分析:肝损伤与CD14表达的关系

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摘要

CD14 is a glycoprotein that recognizes gram-negative bacterial lipopolysaccharide (LPS) and exists in both membrane-bound and soluble forms. Infectious and/or inflammatory diseases induce CD14 expression, which may be involved in the pathology of endotoxin shock. We previously found that the expression of CD14 protein differs among the endotoxin shock models used, although the reasons for these differences are unclear. We hypothesized that the differences in CD14 expression might be due to liver injury, because the hepatic tissue produces CD14 protein. We investigated CD14 expression in the plasma and liver in the carrageenan (CAR)-primed and D-galN-primed mouse models of endotoxin shock. Our results showed that severe liver injury was not induced in CAR-primed endotoxin shock model mice. In this CAR-primed model, the higher mRNA and protein expression of CD14 was observed in the liver, especially in the interlobular bile duct in contrast to D-galN-primed-endotoxin shock model mice. Our findings indicated that the molecular mechanism(s) underlying septic shock in CAR-primed and D-galN-primed endotoxin shock models are quite different. Because CD14 expression is correlated with clinical observations, the CAR-primed endotoxin shock model might be useful for studying the functions of CD14 during septic shock in vivo.
机译:CD14是一种糖蛋白,可识别革兰氏阴性细菌脂多糖(LPS),并以膜结合和可溶性形式存在。传染性和/或炎性疾病诱导CD14表达,这可能与内毒素休克的病理过程有关。我们先前发现,使用的内毒素休克模型之间CD14蛋白的表达有所不同,尽管这些差异的原因尚不清楚。我们假设CD14表达的差异可能是由于肝损伤,因为肝组织产生CD14蛋白。我们调查了角叉菜胶(CAR)启动和D-galN启动的内毒素休克小鼠模型中血浆和肝脏中的CD14表达。我们的结果表明,在CAR引发的内毒素休克模型小鼠中未诱发严重的肝损伤。在这种CAR引发的模型中,与D-galN引发的内毒素休克模型小鼠相比,在肝脏中,尤其是在小叶间胆管中观察到了更高的CD14 mRNA和蛋白表达。我们的发现表明,在CAR引发的和D-galN引发的内毒素休克模型中,败血性休克的分子机制是完全不同的。由于CD14的表达与临床观察结果相关,因此CAR引发的内毒素休克模型对于研究体内败血症性休克期间CD14的功能可能有用。

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