通过白细胞介素-4调节热原诱导的内皮细胞粘附分子(CAMs)的上调:转录机制和CAMs脱落。

Circulatory shock Pub Date : 1994-05-01
S Kapiotis, P Quehenberger, G Sengoelge, C Pärtan, R Eher, H Strobl, D Bevec, D Zapolska, I Schwarzinger, W Speiser
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引用次数: 0

摘要

已知热原白介素1 (IL-1)、肿瘤坏死因子(TNF)和细菌脂多糖(LPS)通过刺激各种粘附分子的表面表达来增加内皮细胞(EC)对白细胞的粘附。IL-4是活化t细胞的产物,可影响热原介导的EC粘附分子表面表达的调节。在本研究中,我们研究了IL-4对热原诱导的人脐静脉EC (HUVEC)细胞粘附分子(CAMs) ICAM-1(细胞间细胞粘附分子-1)、内皮白细胞粘附分子-1 (ELAM-1)和血管细胞粘附分子-1 (VCAM-1)上调的影响。流式细胞术检测粘附分子表面表达,Northern blot检测HUVEC mRNA含量,ELISA检测条件培养基中ICAM-1抗原。IL-1 (100 U/ml)、TNF (500 U/ml)、LPS(10微克/ml)与HUVEC孵生后,ICAM-1、ELAM-1、VCAM-1表面表达显著升高;IL-1导致ICAM-1表达增加约8倍,ELAM-1表面表达增加约13倍,VCAM-1表达增加约4倍。热原与IL-4 (500 U/ml)共孵育对HUVEC表面的促粘作用有不同程度的影响。在IL-4存在的情况下,il -1诱导的ICAM-1上调减少,ELAM-1上调不受IL-4的显著影响,IL-4增强了VCAM-1的诱导。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Modulation of pyrogen-induced upregulation of endothelial cell adhesion molecules (CAMs) by interleukin-4: transcriptional mechanisms and CAM-shedding.

The pyrogens interleukin 1 (IL-1), tumor necrosis factor (TNF), and bacterial lipopolysaccharides (LPS) are known to increase endothelial cell (EC) adhesiveness for leukocytes by stimulating surface expression of various adhesion molecules. IL-4, a product of activated T-cells, was shown to affect pyrogen-mediated regulation of EC adhesion molecule surface expression. In the present study, we investigated the effect of IL-4 on pyrogen-induced upregulation of the cell adhesion molecules (CAMs) ICAM-1 (intercellular cell adhesion molecule-1), ELAM-1 (endothelial leucocyte adhesion molecule-1), and VCAM-1 (vascular cell adhesion molecule-1) in cultured human umbilical vein EC (HUVEC). Surface expression of adhesion molecules was quantified by flow cytometry, HUVEC mRNA content was estimated by Northern blot analysis, and ICAM-1 antigen in conditioned media was measured by ELISA. Incubation of HUVEC with IL-1 (100 U/ml), TNF (500 U/ml), and LPS (10 micrograms/ml) caused significant increase in ICAM-1, ELAM-1, and VCAM-1 surface expression; IL-1 caused about an eightfold increase in ICAM-1 expression, about a 13-fold increase in ELAM-1 surface expression, and about a fourfold increase in VCAM-1 expression. Coincubation of pyrogens with IL-4 (500 U/ml) differentially influenced their proadhesive effects on the HUVEC surface. In the presence of IL-4, IL-1-induced ICAM-1 upregulation was reduced, ELAM-1 upregulation was not significantly influenced by IL-4, and induction of VCAM-1 was enhanced by IL-4.(ABSTRACT TRUNCATED AT 250 WORDS)

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