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首页> 外文期刊>Journal of orthopaedic research >Postoperative serum attenuates LPS-induced release of TNF-alpha in orthopaedic surgery.
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Postoperative serum attenuates LPS-induced release of TNF-alpha in orthopaedic surgery.

机译:术后血清在骨科手术中减弱LPS诱导的TNF-α释放。

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Studies with ex vivo stimulation of whole blood samples from injured patients have revealed a diminished production capacity for a broad range of secretory products, including inflammatory cytokines. Recent interest has focused on the release of mediators in serum that depress the cell-mediated immune response following trauma. The involvement of the lipid mediator prostaglandin E2 (PGE2) has been assumed because it is a potent endogenous immunosuppressor. In the present study, we tested the hypothesis that inhibitory substances circulating in the patient's serum after a major musculoskeletal trauma might impair leukocyte function by evaluating the effect of such serum on cytokine release in a whole blood model. Six females and three males undergoing elective total hip replacement were included in the study. Ex vivo LPS-induced TNF-alpha and IL-10 were measured in whole blood sampled preoperatively and added serum taken before, at the end of operation, and at postoperative days 1 and 6 with saline as negative control. LPS induced significant releases of TNF-alpha and IL-10 in whole blood. Addition of preoperative, postoperative, and day-1 postoperative serum did not alter the LPS-induced release of TNF-alpha as compared to saline. In the presence of serum from postoperative day 6, however, the expression of TNF-alpha was significantly reduced as compared to saline and preoperative serum (p = 0.021 and 0.008, respectively). Neither of the serum samples altered the release of IL-10. PGE2 was significantly (p = 0.008) increased in serum at postoperative day 6 as compared to preoperative levels. In conclusion, these data show that at day 6 after major orthopaedic surgery, the patient serum contained activity that inhibited ex vivo LPS-induced TNF-alpha release. The potent TNF-alpha inhibitory activity found at day 6 after injury correlated with increased levels of PGE2 and indicates cell-mediated hyporesponsiveness to a second stimulus.
机译:对来自受伤患者的全血样品进行离体刺激的研究表明,包括炎症细胞因子在内的多种分泌产物的生产能力正在下降。最近的关注集中在血清中释放介体,其在创伤后抑制细胞介导的免疫反应。已经假定脂质介体前列腺素E2(PGE2)参与其中,因为它是一种有效的内源性免疫抑制剂。在本研究中,我们通过评估全血模型中这种血清对细胞因子释放的影响,检验了一种假设,即在严重的骨骼肌肉骨骼创伤后患者血清中循环的抑制物质可能会损害白细胞功能。这项研究包括接受选择性全髋关节置换的六名女性和三名男性。术前在全血中测量离体LPS诱导的TNF-α和IL-10,并在术前,术中,术后1和6天添加盐水作为阴性对照。 LPS诱导全血中TNF-alpha和IL-10的大量释放。与盐水相比,术前,术后和术后1天血清的添加均未改变LPS诱导的TNF-α释放。但是,从术后第6天开始有血清存在,与盐水和术前血清相比,TNF-α的表达显着降低(分别为p = 0.021和0.008)。血清样品均未改变IL-10的释放。与术前水平相比,术后6天PGE2的血清显着增加(p = 0.008)。总之,这些数据表明,在骨科大手术后的第6天,患者血清中含有抑制离体LPS诱导的TNF-α释放的活性。损伤后第6天发现有效的TNF-α抑制活性与PGE2水平升高相关,并表明细胞介导的对第二种刺激的反应低下。

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