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首页> 外文期刊>Infection and immunity >Endotoxin Binding and Elimination by Monocytes: Secretion of Soluble CD14 Represents an Inducible Mechanism Counteracting Reduced Expression of Membrane CD14 in Patients with Sepsis and in a Patient with Paroxysmal Nocturnal Hemoglobinuria
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Endotoxin Binding and Elimination by Monocytes: Secretion of Soluble CD14 Represents an Inducible Mechanism Counteracting Reduced Expression of Membrane CD14 in Patients with Sepsis and in a Patient with Paroxysmal Nocturnal Hemoglobinuria

机译：内毒素结合和单核细胞消除：可溶性CD14的分泌代表一种诱导的机制，该机制可抵消败血症患者和阵发性夜间血红蛋白尿患者的膜CD14表达降低。

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Little is known about the role of peripheral blood mononuclear cells (PBMCs) in lipopolysaccharide (LPS) elimination. We studied the endotoxin elimination capacities (EEC) of PBMCs of 15 healthy volunteers, 13 patients with sepsis, and 1 patient suffering from paroxysmal nocturnal hemoglobinuria (PNH). Although expression of CD14, the best-characterized receptor for LPS to date, was reduced from 93.6% ± 0.8% in healthy subjects to 50.5% ± 6.5% in patients with sepsis and was 0.3% in a patient with septic PNH, EEC were found to be unchanged. There was no difference in the amount of tumor necrosis factor alpha (TNF-α) released by PBMCs of healthy donors and patients with sepsis. Anti-CD14 antibodies (MEM-18) completely suppressed EEC, binding of fluorescein isothiocyanate-labeled LPS to monocytes as determined by FACScan analysis, and TNF-α release in all three groups studied. The concentrations of soluble CD14 (sCD14) secreted by endotoxin-stimulated PBMCs from healthy donors and patients with sepsis amounted to 4.5 ± 0.4 and 20.1 ± 1.8 ng/ml, respectively. Based on our results, we suggest that PBMCs eliminate LPS by at least two different mechanisms; in healthy subjects, the membrane CD14 (mCD14) receptor is the most important factor for LPS elimination, while in patients with sepsis (including the septic state of PNH), increased sCD14 participates in LPS elimination. Secretion of sCD14 is strongly enhanced under conditions of low expression of mCD14 in order to counteract the reduction of mCD14 and maintain the function of monocytes. This sCD14 may substitute the role of mCD14 in LPS elimination during sepsis. The elimination of LPS by PBMCs correlates with the binding reaction and the secretion of TNF-α.
机译：关于外周血单核细胞（PBMC）在消除脂多糖（LPS）中的作用知之甚少。我们研究了15名健康志愿者，13名败血症患者和1名阵发性夜间血红蛋白尿（PNH）患者的PBMC的内毒素消除能力（EEC）。尽管迄今LPS最具特征的受体CD14的表达从健康受试者的93.6％±0.8％降低至败血症患者的50.5％±6.5％，败血症的PNH，EEC患者为0.3％保持不变。健康供体和败血症患者的PBMC释放的肿瘤坏死因子α（TNF-α）的量没有差异。通过FACScan分析确定，抗CD14抗体（MEM-18）完全抑制EEC，异硫氰酸荧光素标记的LPS与单核细胞的结合，并且在所有三组中均抑制TNF-α的释放。内毒素刺激的PBMC从健康供体和败血症患者体内分泌的可溶性CD14（sCD14）浓度分别为4.5±0.4和20.1±1.8 ng / ml。根据我们的结果，我们建议PBMC通过至少两种不同的机制消除LPS。在健康受试者中，膜CD14（mCD14）受体是消除LPS的最重要因素，而在败血症患者（包括败血症的PNH）中，增加的sCD14参与LPS的消除。为了抵消mCD14的减少并保持单核细胞的功能，在mCD14的低表达的条件下sCD14的分泌被强烈增强。 sCD14可能替代败血症期间mCD14在LPS消除中的作用。 PBMCs消除LPS与结合反应和TNF-α的分泌有关。

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