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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Endotoxin induces rapid metalloproteinase-mediated shedding followed by up-regulation of the monocyte hemoglobin scavenger receptor CD163.
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Endotoxin induces rapid metalloproteinase-mediated shedding followed by up-regulation of the monocyte hemoglobin scavenger receptor CD163.

机译：内毒素诱导快速的金属蛋白酶介导的脱落，然后上调单核细胞血红蛋白清除剂受体CD163。

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摘要

CD163, a monocyte and macrophage-specific surface glycoprotein, which is increased by interleukin-10 and glucocorticoids, is a scavenger receptor for hemoglobin/haptoglobin complexes. We report a rapid and highly reproducible rise in soluble CD163 in the plasma of human volunteers given intravenous lipopolysaccharide (LPS). We also show that LPS induces shedding of CD163 from the surface of isolated monocytes, identifying shedding from monocytes and macrophages as a likely mechanism for the endotoxemia-associated rise in plasma CD163 in vivo. Studies using the inhibitor TAPI-0 indicate that a metalloproteinase is responsible for LPS-mediated shedding of CD163. Finally, we demonstrate a marked increase in surface CD163 expression on circulating monocytes 24 h following experimental endotoxemia. These findings show that CD163 is rapidly mobilized in response to bacterial endotoxin. As hemoglobin can bind LPS and enhance its toxicity, it will be important to determine how cell surface and soluble CD163 influence inflammatory processes during sepsis.
机译：CD163是一种单核细胞和巨噬细胞特异性表面糖蛋白，被白介素10和糖皮质激素增加，是血红蛋白/触珠蛋白复合物的清除剂受体。我们报告了人类自愿者给予静脉内脂多糖（LPS）的血浆中可溶性CD163的快速和高度可再现的增长。我们还显示，LPS诱导单核细胞表面CD163脱落，从单核细胞和巨噬细胞中脱落是内毒素血症相关血浆体内CD163升高的可能机制。使用抑制剂TAPI-0的研究表明，金属蛋白酶负责LPS介导的CD163脱落。最后，我们证明了实验性内毒素血症后24小时循环单核细胞表面CD163表达的明显增加。这些发现表明，CD163响应细菌内毒素而迅速动员。由于血红蛋白可以结合LPS并增强其毒性，因此重要的是确定败血症期间细胞表面和可溶性CD163如何影响炎症过程。

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