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首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Alterations in inflammatory capacity and TLR expression on monocytes and neutrophils after cardiopulmonary bypass.
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Alterations in inflammatory capacity and TLR expression on monocytes and neutrophils after cardiopulmonary bypass.

机译：改变炎症容量和TLR表情后单核细胞和中性粒细胞心肺旁路。

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Cardiopulmonary bypass (CPB) is associated with immune paresis, which predisposes to the development of postoperative sepsis. The aims of this study were to characterize the ex vivo cytokine responses to bacterial cell wall components in whole blood from patients undergoing CPB and to determine whether altered leukocyte expression of Toll-like receptors (TLRs) is involved in immune paresis after CPB. We recruited 6 patients undergoing routine cardiac surgery with CPB. Preoperatively, at the end of CPB and 20 h later, blood was obtained, anticoagulated, and leukocyte surface expression of CD14, TLR2, and TLR4 was quantified by flow cytometry. In addition, blood was incubated at 37 degrees C in the presence of peptidoglycan (PepG) and/or lipopolysaccharide (LPS), and plasma cytokines were measured by enzyme immunoassay. At the end of CPB, ex vivo production of tumor necrosis factor alpha, interleukin (IL) 1beta, IL-8, and IL-10 in response to PepG or LPS was virtually abolished (P < 0.05). The following day, there was recovery of all cytokine responses to PepG. Tumor necrosis factor alpha and IL-1beta responses to LPS partially recovered, whereas IL-8 and IL-10 responses recovered. At the end of CPB, there was more than 50% reduction in neutrophil TLR2 and TLR4 expression (P < 0.05), with recovery to baseline the following day. There was a 29% reduction in monocyte TLR4 expression at the end of CPB (P < 0.05) and more than 120% increase in monocyte TLR2 and 4 expression the following day (P < 0.05). In conclusion, reduced ex vivo production of cytokines cannot be fully accounted for by downregulation of TLR expression, although receptor upregulation may contribute to the later recovery of responsiveness.
机译：体外循环(CPB)相关联易诱发的免疫麻痹性痴呆术后脓毒症的发展。本研究描述了体外细胞因子对细菌细胞壁的反应组件从病人全血发生心脏是否改变白细胞toll样受体的表达(通常)是参与CPB后免疫麻痹性痴呆。我们招募6例接受常规心脏手术体外循环。心脏和20 h以后,血液得到,实际上,白细胞表面表达CD14、TLR2和TLR4被流量化血细胞计数。度的肽聚糖(PepG)和/或脂多糖(LPS)和等离子体细胞因子通过酶免疫分析法测定。体外循环结束时,来自体内的肿瘤坏死因子α,白介素(IL) 1β,引发,il - 10在应对PepG或有限合伙人实际上废除(P < 0.05)。天,有复苏的细胞因子的反应PepG。对有限合伙人的反应部分恢复,而引发和il - 10响应恢复。体外循环,减少50%以上中性粒细胞TLR2和TLR4表达(P < 0.05),第二天恢复到基线。单核细胞TLR4减少29%表达式的心脏(P < 0.05)比增长120%,单核细胞TLR2和4表达式第二天(P < 0.05)。结论体外生产减少不能完全由细胞因子downregulation TLR的表情,虽然受体upregulation可能导致以后复苏的响应能力。

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