Burn-induced heart failure: lipopolysaccharide binding protein improves burn and endotoxin-induced cardiac contractility deficits.
Burn-induced heart failure: lipopolysaccharide binding protein improves burn and endotoxin-induced cardiac contractility deficits.
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DOI：
10.1016/j.jss.2009.06.012
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发表时间：
2011-01
期刊：
影响因子：
--
通讯作者：
Hemmila MR
中科院分区：
文献类型：
--
作者：
Niederbichler AD;Hoesel LM;Ipaktchi K;Olivarez L;Erdmann M;Vogt PM;Su GL;Arbabi S;Westfall MV;Wang SC;Hemmila MR
烧伤常并发细菌感染。烧伤后，暴露于内毒素可导致心肌细胞肌节收缩功能明显下降。脂多糖结合蛋白（Lipopolysaccharide-binding protein，LBP）是一种急性时相蛋白，其通过与脂多糖（lipid A）部分结合而增强对脂多糖（lipopolysaccharide，LPS）的识别。在这项研究中，我们试图确定重组大鼠LBP（rLBP）对烧伤或假损伤后的心肌细胞肌节功能的影响，在存在或不存在细菌内毒素的情况下。大鼠进行全层30%总体表面积烧伤或假烧伤。在损伤后24小时，分离心肌细胞，以50，000个细胞/孔铺板，并与50 μg/mL LPS和rLBP或氯霉素乙酰转移酶（BVCat，使用与rLBP相同的表达系统产生的不相关对照蛋白）以1、5、10和30%的体积浓度孵育。将心肌细胞亚群与5%大鼠血清或30%rLBP孵育，并使用LBP样合成肽（LBPK 95 A）进行阻断实验。使用具有长度检测软件的可变速率视频摄像机系统测量体外肌节功能。在LPS存在下，烧伤和假损伤衍生的心肌细胞与高剂量rLBP的共培养导致单独暴露于LPS后在肌节缩短峰值中观察到的功能障碍显著减少。在LPS存在下，浓度为20 μg/mL的LBP样肽LBPK 95 A消除了30%rLBP和5%大鼠血清将烧伤后分离的心肌细胞的肌节缩短峰值恢复到不存在内毒素暴露时所表现出的功能水平的能力。在烧伤后LPS刺激的情况下，高浓度的rLBP在体外恢复心肌细胞肌节收缩功能。高浓度的rLBP可能导致抑制性结合作用，而不是增强细胞LPS受体复合物对LPS的识别，该抑制性结合作用使热损伤后内毒素暴露对心肌细胞功能的影响最小化。
Burn injury is frequently complicated by bacterial infection. Following burn injury, exposure to endotoxin produces a measurable decrease in cardiomyocyte sarcomere contractile function. Lipopolysaccharide-binding protein (LBP) is an acute phase protein that potentiates the recognition of lipopolysaccharide (LPS) by binding to the lipid A moiety of LPS. In this study we sought to determine the effect of recombinant rat LBP (rLBP) on cardiomyocyte sarcomere function after burn or sham injury in the presence or absence of bacterial endotoxin. Rats underwent a full-thickness 30% total body surface area scald or sham burn. At 24 hours post injury, cardiomyocytes were isolated, plated at 50,000 cells/well and incubated with 50 μg/mL LPS and rLBP) or chloramphenicol acetyltransferase (BVCat, an irrelevant control protein produced using the same expression system as rLBP) at concentrations by volume of 1, 5, 10, and 30%. Subsets of cardiomyocytes were incubated with 5 % rat serum or 30% rLBP and blocking experiments were conducted using an LBP-like synthetic peptide (LBPK95A). In-vitro sarcomere function was measured using a variable rate video camera system with length detection software. Co-culture of burn and sham injury derived cardiomyocytes with high-dose rLBP in the presence of LPS resulted in a significant reduction to the functional impairment observed in peak sarcomere shortening following exposure to LPS alone. LBP-like peptide LBPK95A at a concentration of 20 μg/mL, in the presence of LPS, abolished the ability of 30 % rLBP and 5% rat serum to restore peak sarcomere shortening of cardiomyocytes isolated following burn injury to levels of function exhibited in the absence of endotoxin exposure. In the setting of LPS challenge following burn injury, rLBP at high concentrations restores cardiomyocyte sarcomere contractile function in vitro. Rather than potentiating the recognition of LPS by the cellular LPS receptor complex, rLBP at high concentrations likely results in an inhibitory binding effect that minimizes the impact of endotoxin exposure on cardiomyocyte function following thermal injury.
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影响因子：
15.9
作者：
Lamping, N;Dettmer, R;Schumann, RR
通讯作者：
Schumann, RR
影响因子：
37.8
作者：
Knuefermann, P;Nemoto, S;Vallejo, JG
通讯作者：
Vallejo, JG
影响因子：
6.4
作者：
FROON, AHM;DENTENER, MA;BUURMAN, WA
通讯作者：
BUURMAN, WA
DOI：
10.1097/00004630-200021040-00010
发表时间：
2000-07-01
期刊：
JOURNAL OF BURN CARE & REHABILITATION
影响因子：
--
作者：
Klein, RD;Su, GL;Wang, SC
通讯作者：
Wang, SC
影响因子：
3.1
作者：
SEATTER, SC;LI, MH;WEST, MA
通讯作者：
WEST, MA