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首页> 外文期刊>Infection and immunity >Killed Escherichia coli stimulates macrophage-mediated alterations in hepatocellular function during in vitro coculture: a mechanism of altered liver function in sepsis.
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Killed Escherichia coli stimulates macrophage-mediated alterations in hepatocellular function during in vitro coculture: a mechanism of altered liver function in sepsis.

机译：被杀死的大肠杆菌在体外共培养过程中刺激巨噬细胞介导的肝细胞功能改变：败血症中肝功能改变的机制。

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Hepatic dysfunction is a poorly understood and highly lethal component of multiple-system organ failure. Both in vivo and in vitro studies of "liver" function have generally neglected hepatocyte-Kupffer cell interactions. In the following experiments, isolated hepatocytes were cocultivated with unstimulated peritoneal cells, predominately macrophages, which served as a readily available Kupffer cell analog. Coculture of hepatocytes with peritoneal cells resulted in little or no change in [3H]leucine incorporation into hepatocyte protein. When gentamicin-killed Escherichia coli cells (GKEC) were added to coculture, there was a marked decrease in hepatocyte [3H]leucine incorporation. In contrast, GKEC added to hepatocytes alone had no effect. Kinetic data revealed an 8-h delay before any significant decrease in leucine incorporation into hepatocyte protein after the addition of GKEC to the coculture. The maximal decrease in hepatocyte [3H]leucine incorporation occurred 24 h after GKEC were added. The decrease observed 24 h after GKEC were added disappeared almost completely after 48 h of coculture. Similar alterations in cocultured hepatocyte protein synthesis were observed after the addition of phorbol myristate acetate, lipopolysaccharide, or muramyl dipeptide, a component of bacterial peptidoglycan. Hepatocyte viability by trypan blue exclusion was unchanged, and gross morphology by light or electron microscopy was unaffected. We propose that during sepsis, macrophages (Kupffer cells) respond to circulating microbial products and mediate alterations in hepatocyte function. These experiments underscore the important role of Kupffer cell function in attempts to understand hepatic malfunction in multiple-system organ failure.
机译：肝功能障碍是多系统器官衰竭的一个鲜为人知且高度致死的成分。体内和体外对“肝”功能的研究通常都忽略了肝细胞-库普弗细胞的相互作用。在以下实验中，将分离出的肝细胞与未经刺激的腹膜细胞（主要是巨噬细胞）共培养，用作容易获得的库普弗细胞类似物。肝细胞与腹膜细胞的共培养导致[3H]亮氨酸掺入肝细胞蛋白质的变化很小或没有变化。当将庆大霉素杀死的大肠杆菌细胞（GKEC）添加到共培养物中时，肝细胞[3H]亮氨酸的掺入显着减少。相反，仅将GKEC加入肝细胞没有作用。动力学数据显示，在共培养物中加入GKEC后，亮氨酸掺入肝细胞蛋白质的任何显着减少之前，都要延迟8小时。加入GKEC后24小时，肝细胞[3H]亮氨酸的掺入量最大减少。共培养48小时后，添加GKEC 24小时后观察到的减少几乎完全消失。在加入佛波醇肉豆蔻酸酯乙酸盐，脂多糖或鼠李糖基二肽（细菌肽聚糖的一种成分）后，在共培养的肝细胞蛋白质合成中观察到类似的变化。锥虫蓝排除后的肝细胞活力未改变，光或电子显微镜观察的总体形态未受影响。我们建议在脓毒症期间，巨噬细胞（库普弗细胞）对循环的微生物产物作出反应并介导肝细胞功能的改变。这些实验强调了库普弗细胞功能在理解多系统器官衰竭中的肝功能衰竭中的重要作用。

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