Thermotolerance protects against endotoxin-mediated microvascular injury
Thermotolerance protects against endotoxin-mediated microvascular injury
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DOI：
10.1006/jsre.2000.5896
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发表时间：
2001-02-01
影响因子：
2.2
通讯作者：
Bouchier-Hayes, D
中科院分区：
文献类型：
--
作者：
Chen, G;Kelly, C;Bouchier-Hayes, D
内毒素诱导的组织损伤的早期事件是白细胞通过内皮的粘附和迁移。这是一个三阶段的过程，最初是低级选择素介导的粘附，表现为滚动速度的降低，随后是整合素介导的粘附和迁移。热耐受性已被证明可以减少内毒素诱导的组织损伤和死亡率。本研究的目的是探讨热耐受性对白细胞-内皮细胞相互作用的影响。活体视频显微镜检查血流动力学参数，白细胞滚动，粘附和迁移在大鼠肠系膜毛细血管后微静脉。Sprague-Dawley大鼠随机分为对照组、脂多糖（LPS）组和热耐受+ LPS组。在LPS给药前18 h，通过将核心体温升高至41 ± 0.5 ℃持续15 min诱导热耐受性。在基线记录后，通过颈静脉给药LPS（055：B5 15 mg/kg）。在基线0 min和LPS给药后10、30、60和90 min，通过活体显微镜测量白细胞滚动速度和粘附和迁移的白细胞数量。用Western免疫印迹法检测组织中热休克蛋白72（HSP 72）的表达。结果表明，LPS给药显著降低了内毒素血症时白细胞的滚动速度，并增加了白细胞粘附（10.3 +/- 1.67、13.2 +/- 1.40和10.0 +/- 1.57/100 μ m）和迁移（5.7 +/- 1.02和8.3 +/- 1.76/视野）（与基线和对照组相比P < 0.01）。热耐受性维持了白细胞滚动速度，并在LPS给药后30和60 min显著降低了白细胞粘附（5.7 ± 0.88和4.0 ± 0.68/100 m）和迁移（2.8 ± 0.32和3.0 ± 0.68/视野）（P < 0.01和0.05 vs LPS组）。热耐受诱导肠系膜、肠和肺中HSP 72的表达。这项研究表明，热耐受性通过减少白细胞-内皮细胞粘附和迁移来减弱LPS诱导的微血管损伤，（C）2000学术出版社。
An early event in endotoxin-induced tissue injury is adhesion and migration of leukocytes through the endothelium. This is a three-stage process, initially low-grade selectin-mediated adhesion, seen as a decrease in rolling velocity, followed by integrin-mediated adhesion and transmigration. Thermotolerance has been shown to reduce tissue injury and mortality induced by endotoxin. The aim of this study was to investigate the effect of thermotolerance on leukocyte-endothelial interactions. Intravital video microscopy was used to examine hemodynamic parameters, leukocyte rolling, adhesion, and migration in rat mesenteric postcapillary venules. Sprague-Dawley rats were randomized into control, lipopolysaccharide (LPS), and thermotolerance + LPS groups. Thermotolerance was induced 18 h prior to administration of LPS by elevating core body temperature to 41 + 0.5 degreesC for 15 min. LPS (055:B5 15 mg/kg) was administered via the jugular vein after baseline recording. Leukocyte rolling velocity and the number of adherent and migrated leukocytes were measured by intravital microscopy at baseline 0 min and 10, 30, 60, and 90 min after LPS administration. Heat shock protein 72 (HSP72) expression in tissues was determined by Western immunoblotting. The results indicated that LPS administration significantly decreased leukocyte rolling velocity during endotoxemia and increased leukocyte adhesion (10.3 +/- 1.67, 13.2 +/- 1.40, and 10.0 +/- 1.57/100 mum) and migration (5.7 +/- 1.02 and 8.3 +/- 1.76/field) at 30, 60, and 90 min after LPS injection (P < 0.01 vs baseline and control group). Thermotolerance maintained leukocyte rolling velocity and significantly reduced leukocyte adhesion (5.7 +/- 0.88 and 4.0 +/- 0.68/100 m) and migration (2.8 +/- 0.32 and 3.0 +/- 0.68/field) at 30 and 60 min after LPS administration (P < 0.01 and 0.05 vs LPS group). Expression of HSP72 was induced in mesentery, gut, and lung by thermotolerance. This study indicates that thermotolerance attenuated LPS-induced microvascular injury by decreasing leukocyte-endothelial adhesion and migration, (C) 2000 Academic Press.