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首页> 外文期刊>Alcoholism: Clinical and experimental research >Phosphatidylcholine reverses ethanol-induced increase in transepithelial endotoxin permeability and abolishes transepithelial leukocyte activation.
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Phosphatidylcholine reverses ethanol-induced increase in transepithelial endotoxin permeability and abolishes transepithelial leukocyte activation.

机译：磷脂酰胆碱可逆转乙醇诱导的跨上皮内毒素通透性增加，并消除跨上皮白细胞激活。

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BACKGROUND: Chronic alcohol abuse increases both intestinal bacterial overgrowth and intestinal permeability to macromolecules. Intestinal permeability of endotoxin, a component of the outer cell membrane of Gram-negative bacteria, plays a crucial role in the development of alcohol-induced liver disease (ALD). As impaired bile flow leads to endotoxemia and the bile component phosphatidylcholine (PC) is therapeutically active in ALD, we tested the hypothesis that conjugated primary bile salts (CPBS) and PC inhibit ethanol-enhanced transepithelial permeability of endotoxin and the subsequent transepithelial activation of human leukocytes. METHODS: For this purpose, we used a model in which intestinal epithelial cells (Caco-2) were basolaterally cocultivated with mononuclear leukocytes. Cells were challenged apically with endotoxin from Escherichia coli K12 and were incubated with or without the addition of CPBS (1.5 mM), PC (0.38 mM), pooled human bile (2%) in combination with ethanol (0 to 66 mM). RESULTS: Ethanol decreased integrity of intestinal epithelial cell monolayer and enhanced transepithelial permeability of endotoxin. Both the transepithelial permeability of endotoxin and the transepithelial stimulation of leukocytes were nearly completely abolished after the apical supplementation of PC with CPBS, but not by CPBS alone. Ethanol up to 66 mM was not able to reverse this effect. CONCLUSIONS: A considerable part of the therapeutic and preventive effect of PC supplementation in ALD might result from a reduction of ethanol-enhanced permeability of endotoxin through the intestinal barrier.
机译：背景：长期酗酒会增加肠道细菌的过度生长和肠道对大分子的渗透性。内毒素是革兰氏阴性细菌外细胞膜的一个组成部分，其肠道通透性在酒精诱导的肝病（ALD）的发展中起着至关重要的作用。由于胆汁流量受损导致内毒素血症并且胆汁成分磷脂酰胆碱（PC）在ALD中具有治疗活性，因此我们测试了以下假设：共轭初级胆汁盐（CPBS）和PC抑制乙醇增强内毒素的跨上皮通透性以及随后的人的上皮激活白细胞。方法：为此，我们使用了一种模型，其中将肠上皮细胞（Caco-2）与单核白细胞在基底外侧共培养。用来自大肠杆菌K12的内毒素对细胞进行顶攻，并在添加或不添加CPBS（1.5 mM），PC（0.38 mM），合并的人胆汁（2％）与乙醇（0至66 mM）的情况下进行孵育。结果：乙醇降低了肠上皮细胞单层的完整性并增强了内毒素的经上皮通透性。在顶端添加CPBS而不是单独使用CPBS后，内毒素的上皮通透性和白细胞的上皮刺激几乎都被消除了。高达66 mM的乙醇无法逆转这种影响。结论：PC补充剂对ALD的治疗和预防作用中，相当一部分可能是由于乙醇增强的内毒素通过肠屏障的渗透性降低所致。

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