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首页> 外文期刊>Infection and immunity >New Scavenger Receptor-Like Receptors for the Binding of Lipopolysaccharide to Liver Endothelial and Kupffer Cells
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New Scavenger Receptor-Like Receptors for the Binding of Lipopolysaccharide to Liver Endothelial and Kupffer Cells

机译：脂多糖与肝内皮细胞和库普弗细胞结合的新型清道夫受体样受体

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Lipopolysaccharide (LPS) is cleared from the blood mainly by the liver. The Kupffer cells are primarily responsible for this clearance; liver endothelial and parenchymal cells contribute to a lesser extent. Although several binding sites have been described, only CD14 is known to be involved in LPS signalling. Among the other LPS binding sites that have been identified are scavenger receptors. Scavenger receptor class A (SR-A) types I and II are expressed in the liver on endothelial cells and Kupffer cells, and a 95-kDa receptor, identified as macrosialin, is expressed on Kupffer cells. In this study, we examined the role of scavenger receptors in the binding of LPS by the liver in vivo and in vitro. Fucoidin, a scavenger receptor ligand, significantly reduced the clearance of 125I-LPS from the serum and decreased the liver uptake of 125I-LPS about 40%. Within the liver, the in vivo binding of 125I-LPS to Kupffer and liver endothelial cells was decreased 72 and 71%, respectively, while the binding of 125I-LPS to liver parenchymal cells increased 34% upon fucoidin preinjection. Poly(I) inhibited the binding of 125I-LPS to Kupffer and endothelial cells in vitro 73 and 78%, respectively, while poly(A) had no effect. LPS inhibited the binding of acetylated low-density lipoprotein (acLDL) to Kupffer and liver endothelial cells 40 and 55%, respectively, and the binding of oxidized LDL (oxLDL) to Kupffer and liver endothelial cells 65 and 61%, respectively. oxLDL and acLDL did not significantly inhibit the binding of LPS to these cells. We conclude that on both endothelial cells and Kupffer cells, LPS binds mainly to scavenger receptors, but SR-A and macrosialin contribute to a limited extent to the binding of LPS.
机译：脂多糖（LPS）主要通过肝脏从血液中清除。库普弗细胞主要负责清除。肝内皮细胞和实质细胞的贡献程度较小。尽管已经描述了几个结合位点，但是已知只有CD14参与LPS信号传导。在其他已确定的LPS结合位点中，还有清道夫受体。 I型和II型清道夫受体在肝脏中的内皮细胞和Kupffer细胞上表达，而识别为大唾液酸蛋白的95 kDa受体在Kupffer细胞上表达。在这项研究中，我们研究了体内和体外肝脏中清道夫受体在脂多糖结合中的作用。 Fucoidin是一种清除剂受体配体，可显着降低血清中 125 I-LPS的清除率，并使 125 I-LPS的肝脏吸收降低约40％。在肝脏中， 125 I-LPS与Kupffer和肝内皮细胞的体内结合分别降低72％和71％，而 125 I-LPS与之结合注射岩藻依定素后，肝实质细胞中的总胆固醇增加了34％。 Poly（I）在体外分别抑制 125 I-LPS与Kupffer和内皮细胞的结合73％和78％，而poly（A）没有作用。 LPS分别抑制乙酰化低密度脂蛋白（acLDL）与Kupffer和肝内皮细胞的结合40和55％，以及氧化LDL（oxLDL）与Kupffer和肝内皮细胞的结合65和61％。 oxLDL和acLDL没有明显抑制LPS与这些细胞的结合。我们得出结论，在内皮细胞和库普弗细胞上，LPS主要与清道夫受体结合，但SR-A和大唾液酸蛋白在有限程度上有助于LPS的结合。

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