Parenteral nutrition alters monocyte TNF receptor activity.
Parenteral nutrition alters monocyte TNF receptor activity.
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肠外营养改变单核细胞 TNF 受体活性。
DOI：
10.1006/jsre.1995.1127
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Lowry,SF
中科院分区：
文献类型：
--
作者：
Braxton,CC;Coyle,SM;Montegut,WJ;vanderPoll,T;Roth,M;Calvano,SE;Lowry,SF
据报道，营养供给途径会影响患者群体和正常受试者宿主炎症反应的某些方面。肿瘤坏死因子受体系统是一个复杂的调节机制，可调节肿瘤坏死因子（TNF）的生物利用度。我们试图确定维持全肠外营养（TFN）是否可以改变宿主对内毒素挑战的反应，特别是因为它与 TNF 受体系统有关。 17 名健康男性在静脉输注内毒素（批次 EC-5，20 U/kg）之前随机接受 TPN（n = 8）或特定配方肠内饮食（ENT，n = 9）。与维持肠内营养支持的受试者相比，接受 1 周前 TPN 的受试者在 LPS 后表现出心率和体温升高以及平均动脉压降低。 TPN 受试者对内毒素的反应还表现出相对较高的 TNF 和白细胞介素 6 水平。 LPS 后两组的单核细胞 TNF 受体水平均下降，但 TPN 受试者的这种功能性膜相关 TNF 受体的表达始终较高。 LPS 后，TPN 受试者中可溶性肿瘤坏死因子受体 II (sTNFr II，p75) 的峰值比耳鼻喉科受试者高三倍。相反，肠内喂养组的 sTNFr I (p55) 较高。从这些研究看来，先前的 TPN 不仅影响内毒素的临床表现，而且还调节所有相关 TNF 受体的调节和可溶性受体的脱落。
The route of nutrient provision has been reported to influence some aspects of the host inflammatory response in both patient populations and normal subjects. The tumor necrosis factor receptor system is a complex regulatory mechanism that modulates the bioavailability of tumor necrosis factor (TNF). We sought to determine whether maintenance on total parenteral nutrition (TFN) can alter host response to endotoxin challenge, specifically as it relates to the TNF receptor system. Seventeen healthy men were randomized to receive either TPN (n = 8) or a defined formula enteral diet (ENT, n = 9) prior to intravenous infusion of endotoxin (Lot EC-5, 20 U/kg). The subjects that received 1 week of antecedent TPN exhibited an increased heart rate and temperature and decreased mean arterial pressure post-LPS compared to those subjects maintained on enteral nutritional support. The TPN subjects also exhibited comparatively higher TNF and interleukin-6 levels in response to endotoxin. Monocyte TNF receptor levels decreased in both groups post-LPS, but TPN subjects exhibited consistently greater expression of this functional membrane-associated TNF receptor. After LPS, soluble tumor necrosis factor receptor II (sTNFr II, p75) peaked three times higher in TPN subjects than in ENT subjects. Conversely, sTNFr I (p55) was higher in the enterally fed group. From these studies it appears that antecedent TPN not only influences clinical manifestations of endotoxin but also modulates the regulation of all associated TNF receptors and shedding of soluble receptors.