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The Protective Effects of Lactoferrin Feeding against Endotoxin Lethal Shock in Germfree Piglets

机译:饲喂乳铁蛋白对无胚仔猪内毒素致死性休克的保护作用

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The unique germfree, colostrum-deprived, immunologically “virgin” piglet model was used to evaluate the ability of lactoferrin (LF) to protect against lethal shock induced by intravenously administered endotoxin. Piglets were fed LF or bovine serum albumin (BSA) prior to challenge with intravenousEscherichia coli lipopolysaccharide (LPS), and temperature, clinical symptoms, and mortality were tracked for 48 h following LPS administration. Prefeeding with LF resulted in a significant decrease in piglet mortality compared to feeding with BSA (16.7 versus 73.7% mortality, P < 0.001). Protection against the LPS challenge by LF was also correlated with both resistance to induction of hypothermia by endotoxin and an overall increase in wellness, as quantified by a toxicity score developed for these studies. In vitro studies using a flow cytometric assay system demonstrated that LPS binding to porcine monocytes was inhibited by LF in a dose-dependent fashion, suggesting that the mechanism of LF action in vivo may be inhibition of LPS binding to monocytes/macrophages and, in turn, prevention of induction of monocyte/macrophage-derived inflammatory-toxic cytokines.
机译:独特的无菌,初乳剥夺,免疫学上“纯净”的仔猪模型用于评估乳铁蛋白(LF)预防静脉内注射内毒素引起的致命性休克的能力。给小猪喂LF或牛血清白蛋白(BSA),然后用静脉内的大肠杆菌脂多糖(LPS)攻击,并在LPS给药后48小时追踪温度,临床症状和死亡率。与BSA相比,LF预先喂养导致仔猪死亡率显着降低(死亡率分别为16.7和73.7%, P <0.001)。 LF对LPS攻击的保护作用还与内毒素诱导的体温过低的抵抗力和健康的总体提高有关,这是由针对这些研究开发的毒性评分所量化的。使用流式细胞仪系统进行的体外研究表明,LF以剂量依赖性方式抑制LPS与猪单核细胞的结合,这表明LF在体内的作用机制可能是LPS与单核细胞/巨噬细胞结合的抑制,进而,防止诱导单核细胞/巨噬细胞衍生的炎性毒性细胞因子。

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