INTERLEUKIN-1 ACTS ON CULTURED HUMAN VASCULAR ENDOTHELIUM TO INCREASE THE ADHESION OF POLYMORPHONUCLEAR LEUKOCYTES, MONOCYTES, AND RELATED LEUKOCYTE CELL-LINES
INTERLEUKIN-1 ACTS ON CULTURED HUMAN VASCULAR ENDOTHELIUM TO INCREASE THE ADHESION OF POLYMORPHONUCLEAR LEUKOCYTES, MONOCYTES, AND RELATED LEUKOCYTE CELL-LINES
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DOI：
10.1172/jci112200
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发表时间：
1985-01-01
影响因子：
15.9
通讯作者：
GIMBRONE, MA
中科院分区：
文献类型：
--
作者：
BEVILACQUA, MP;POBER, JS;GIMBRONE, MA
增加的白细胞粘附到血管的内皮衬里是炎症和某些血管疾病的发病机制中的重要事件。我们已经研究了白细胞介素1（IL-1），炎症/免疫介质，内皮细胞-白细胞粘附的影响，使用定量体外试验。用IL-1（5 U/ml 4小时）选择性预处理培养的人脐静脉内皮单层，结果为18.3 ± 0.001。2.6-人外周血多形核白细胞（PMN）粘附的增加倍数（平均值± 0. SEM，n = 16）和2.6 . ±. 0.3-单核细胞粘附的增加倍数（n = 7）超过基础水平。IL-1处理的内皮细胞单层也支持早幼粒细胞系HL-60和单核细胞样细胞系UP 37的粘附增加（33.0 ± 0.01）。6.0倍，n = 6和4.9 ±。0.5倍，n = 15）。相反，白细胞的选择性IL-1预处理，或在粘附试验中加入IL-1，并没有改变内皮细胞-白细胞粘附。条件培养基从IL-1处理的内皮细胞培养也没有促进白细胞粘附到未经处理的单层。IL-1对内皮粘附性的诱导是浓度依赖性的（最大值，10 U/ml）、时间依赖性的（峰值，4-6 h）和可逆的，被放线菌酮（10 μ g/ml）或放线菌素D（5 μ g/ml）阻断，但不被乙酰水杨酸（100 μ M）阻断，并且在没有可检测到的内皮细胞损伤的情况下发生。IL-1处理SV 40转化的人内皮细胞和真皮成纤维细胞并没有增加它们对白细胞的粘附性。这些数据表明，IL-1可以选择性地作用于人血管内皮细胞，以增加其对循环血液白细胞的粘附性，从而在体内炎症部位定位白细胞-血管壁相互作用。
Increased leukocyte adhesion to the endothelial lining of blood vessels is an essential event in inflammation and the pathogenesis of certain vascular diseases. We have studied the effect of interleukin 1 (IL-1), an inflammatory/immune mediator, on endothelial-leukocyte adhesion using quantitative in vitro assays. Selective pretreatment of cultured human umbilical vein endothelial monolayers with IL-1 (5 U/ml 4 h) resulted in an 18.3 .+-. 2.6-fold increase in human peripheral blood polymorphonuclear leukocyte (PMN) adhesion (mean .+-. SEM, n = 16) and a 2.6 .+-. 0.3-fold increase in monocyte adhesion (n = 7) over basal levels. IL-1-treated endothelial monolayers also supported increased adhesion of the promyelocytic cell line HL-60 and the monocytelike cell line UP37 (33.0 .+-. 6.0-fold, n = 6 and 4.9 .+-. 0.5-fold, n = 15, respectively). In contrast, selective IL-1 pretreatment of leukocytes, or the addition of IL-1 during the adhesion assay, did not alter endothelial-leukocyte adhesion. Conditioned medium from IL-1-treated endothelial cultures also did not promote leukocyte adhesion to untreated monolayers. IL-1 induction of endothelial adhesivity was concentration dependent (maximum, 10 U/ml), time dependent (peak, 4-6 h), and reversible, was blocked by cycloheximide (10 .mu.g/ml) or actinomycin D (5 .mu.g/ml) but not by acetylsalicylic acid (100 .mu.M), and occurred without detectable endothelial cell damage. IL-1 treatment of SV40-transformed human endothelial cells and dermal fibroblasts did not increase their adhesivity for leukocytes. These data suggest that IL-1 can act selectively on human vascular endothelium to increase its adhesivity for circulating blood leukocytes, and thus to localize leukocyte-vessel wall interactions at sites of inflammation in vivo.