Migration of neutrophils across endothelial monolayers is stimulated by treatment of the monolayers with interleukin-1 or tumor necrosis factor-alpha.
Migration of neutrophils across endothelial monolayers is stimulated by treatment of the monolayers with interleukin-1 or tumor necrosis factor-alpha.
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DOI：
10.4049/jimmunol.143.10.3309
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发表时间：
1989-11
影响因子：
4.4
通讯作者：
M. Furie;D. McHugh
中科院分区：
文献类型：
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作者：
M. Furie;D. McHugh
为了研究细胞因子IL-1和TNF-α对中性粒细胞跨内皮迁移的影响，将人脐静脉内皮细胞（HUVEC）在由人羊膜制备的结缔组织上生长至汇合。用rIL-1 β（7.5 ng/ml）或rTNF-α（5 ng/ml）预处理HUVEC-羊膜培养物4 h，导致20%至50%的随后加入的中性粒细胞快速迁移穿过内皮单层。相比之下，在没有任何刺激的情况下，只有3 +/-3%的添加的中性粒细胞穿透HUVEC单层。迁移穿过经苦参碱处理的HUVEC的中性粒细胞的数量与响应于FMLP梯度而穿过未经处理的单层的数量相似;此外，它仅比响应于白三烯B4而迁移的中性粒细胞的数量少35%。当HUVEC的细胞因子预处理和趋化梯度诱导迁移时，未观察到一致的累加效应。在IL-1处理的培养物中迁移的中性粒细胞数量与在2.5 × 10（5）至4 × 10（6）中性粒细胞范围内添加的数量成比例。当在最佳浓度下使用时，IL-1和TNF-α在刺激中性粒细胞迁移方面同样有效;当HUVEC用最佳剂量的两种细胞因子一起预处理时，未观察到累加效应。直接加入IL-1或TNF-α的1小时迁移试验没有影响中性粒细胞粘附或迁移通过HUVEC，无论是在存在或不存在的趋化梯度。在该系统中，中性粒细胞跨内皮迁移的刺激似乎不是由羊膜组织对细胞因子的吸附引起的，也不是由于LPS对细胞因子制剂的污染。这些结果表明，在炎症部位产生的IL-1和TNF-α可能作用于内皮细胞，促进中性粒细胞从血管系统中移出。
To study the effects of the cytokines IL-1 and TNF-alpha on the transendothelial migration of neutrophils, human umbilical vein endothelial cells (HUVEC) were grown to confluence on connective tissue prepared from human amniotic membrane. Pretreatment of HUVEC-amnion cultures with rIL-1 beta (7.5 ng/ml) or rTNF-alpha (5 ng/ml) for 4 h resulted in rapid migration of from 20 to 50% of subsequently added neutrophils across the endothelial monolayer. In contrast, only 3 +/- 3% of added neutrophils penetrated the HUVEC monolayer in the absence of any stimulus. The number of neutrophils that migrated across cytokine-treated HUVEC was similar to the number that traversed untreated monolayers in response to gradients of FMLP; in addition, it was only 35% less than the number of neutrophils that migrated in response to leukotriene B4. No consistent additive effect was seen when migration was induced by both cytokine pretreatment of the HUVEC and a chemotactic gradient. The number of neutrophils that migrated across IL-1-treated cultures was proportional to the number added over the range of 2.5 x 10(5) to 4 x 10(6) neutrophils. When used at optimal concentrations, IL-1 and TNF-alpha were equally effective in stimulating neutrophil migration; no additive effect was seen when HUVEC were pretreated with optimal doses of both cytokines together. Direct addition of IL-1 or TNF-alpha to a 1-h migration assay had no effect on neutrophil adhesion to or migration across HUVEC, either in the presence or absence of a chemotactic gradient. Stimulation of neutrophil transendothelial migration in this system did not appear to be caused by adsorption of cytokine by the amniotic tissue, nor was it due to contamination of the cytokine preparations by LPS. These results suggest that IL-1 and TNF-alpha, generated at sites of inflammation, may act upon the endothelium to promote emigration of neutrophils from the vasculature.