Endotoxin enhancement of lymphocyte adherence to cultured sheep lung microvascular endothelial cells.
Endotoxin enhancement of lymphocyte adherence to cultured sheep lung microvascular endothelial cells.
复制标题
内毒素增强淋巴细胞对培养的羊肺微血管内皮细胞的粘附。
DOI：
10.1165/ajrcmb/7.1.81
复制
发表时间：
1992
影响因子：
6.4
通讯作者：
Meyrick,B
中科院分区：
文献类型：
--
作者：
Jones,M;Hoover,R;Meyrick,B
成人呼吸窘迫综合征最常见的诱发因素是革兰氏阴性脓毒症。我们以前的研究表明，单次输注大肠杆菌内毒素到绵羊体内会导致肺微循环中淋巴细胞的早期隔离。本研究观察了内毒素对绵羊淋巴细胞与绵羊肺微血管内皮细胞粘附的影响。内皮细胞暴露于内毒素，随后在单层粘附试验中测量51 Cr标记的淋巴细胞的粘附。内毒素以时间和剂量依赖性方式增强从血液和尾纵隔淋巴结（CMN）淋巴中分离的淋巴细胞的粘附。CMN淋巴细胞的粘附性在用1 pg/ml内毒素处理4 h后从对照值13.6±1.6%增加到29.9±3.1%。两种带状T淋巴细胞均有助于粘附的增加。放线菌酮预处理的内皮细胞显示，内毒素增强的粘附部分依赖于蛋白质的合成。形态学研究表明，增强的粘附性伴随着内皮细胞之间淋巴细胞迁移的5倍增加。与人脐静脉内皮细胞相反，已知的淋巴细胞粘附分子，淋巴细胞功能相关抗原（LFA-I），CD-44和淋巴细胞归巢受体（LECAM-I）的抗体，在阻断绵羊肺内皮细胞的粘附是无效的。我们的结论是，给予内毒素后绵羊肺微循环中淋巴细胞的急性隔离是由于内皮细胞粘附性增加所致。我们的数据表明，这种粘附是由尚未描述的机制介导的，这些机制可能是肺微血管内皮细胞所独有的。成人呼吸窘迫综合征（ARDS）是由各种各样的肺损伤引起的，但最常见的诱发因素是革兰氏阴性脓毒症（1）。通过单次输注大肠杆菌内毒素（革兰氏阴性细菌细胞包膜的一种成分），可以在绵羊中模拟ARDS的结构和生理特征（2）。绵羊输注内毒素后，在肺水肿发生前，肺微循环中的白细胞（中性粒细胞和淋巴细胞）被隔离。虽然中性粒细胞在内毒素诱导的急性肺损伤中的作用已被广泛研究，
The most common predisposing factor for development of the adult respiratory distress syndrome is gramnegative sepsis. Our previous studies have shown that a single infusion of Escherichia coli endotoxin into sheep causes early sequestration of lymphocytes in the lungs' microcirculation. In this report, we examined the effects of endotoxin on sheep lymphocyte adherence to sheep pulmonary microvascular endothelial cells in vitro. Endothelial cells were exposed to endotoxin, and subsequent adherence of 51Cr-Iabeled lymphocytes was measured in a monolayer adhesion assay. Endotoxin enhanced adherence of lymphocytes isolated from blood and caudal mediastinal node (CMN) lymph in a time-and dose-dependent manner. Adherence of CMN lymphocytes increased from a control value of 13.6±1.6% to 29.9±3.1% after 4 h of treatment with 1 pg/mlendotoxin. Both Band T lymphocytes contributed to the increased adherence. Pretreatment of the endothelial cells with cycloheximide revealed that the endotoxin-enhanced adherence was partially dependent upon protein synthesis. Morphologic studies revealed that enhanced adherence was accompanied by a 5-fold increase in migration of lymphocytes between endothelial cells. In contrast to human umbilical vein endothelial cells, antibodies to the known lymphocyte adherence molecules, lymphocyte function-associated antigen (LFA-I), CD-44, and the lymphocyte homing receptor (LECAM-I), were ineffective in blocking adherence to the sheep pulmonary endothelial cells. We conclude that the acute sequestration of lymphocytes in the pulmonary microcirculation of sheep after endotoxin administration is due to increased adhesive properties of the endothelial cells. Our data suggest that this adherence is mediated by as yet undescribed mechanisms that may be unique to pulmonary microvascular endothelium.The adult respiratory distress syndrome (ARDS) results from a wide variety of insults to the lung, but the most common predisposing factor is gram-negative sepsis (1). Structural and physiological characteristics of ARDS can be mimicked in sheep given a single infusion of Escherichia coli endotoxin, a component of the gram-negative bacterial cell envelope (2). After endotoxin infusion into sheep, there is sequestration of leukocytes, both neutrophils and lymphocytes, in the microcirculation of the lungs before the onset of pulmonary edema. Although the role of the neutrophil in endotoxin-induced acute lung injury has been extensively in-