IL‐1 activation of endothelium supports VLA‐4 (CD49d/CD29)‐mediated monocyte transendothelial migration to C5a, MIP‐1α, RANTES, and PAF but inhibits migration to MCP‐1: a regulatory role for endothelium‐derived MCP‐1
IL‐1 activation of endothelium supports VLA‐4 (CD49d/CD29)‐mediated monocyte transendothelial migration to C5a, MIP‐1α, RANTES, and PAF but inhibits migration to MCP‐1: a regulatory role for endothelium‐derived MCP‐1
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IL-1 内皮激活支持 VLA-4 (CD49d/CD29) 介导的单核细胞跨内皮迁移至 C5a、MIP-1α、RANTES 和 PAF，但抑制迁移至 MCP-1：内皮源性 MCP-1 的调节作用
DOI：
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发表时间：
1995
影响因子：
5.5
通讯作者：
A. Issekutz
中科院分区：
文献类型：
--
作者：
H. Chuluyan;T. Schall;T. Yoshimura;A. Issekutz
我们研究了白细胞介素-1（IL-1）激活人脐静脉内皮细胞（HUVE）对趋化因子诱导的人单核细胞跨内皮迁移的影响。针对单核细胞上CD 11/CD 18复合物的CD 18的单克隆抗体（mAb; 60.3）完全抑制（90%）单核细胞对巨噬细胞炎性蛋白-1 α（MIP-1α）、RANTES、血小板活化因子（PAF）或单核细胞趋化蛋白-1（MCP-1）的反应，并部分抑制（75%）对C5 a的反应。当用IL-1 α刺激HUVE（5 h，0.1 ng/ml）时，CD 18 mAb不再抑制单核细胞对C5 a、MIP-1 α、RANTES或PAF的迁移反应。然而，针对极晚期抗原4（CD 49 d（/CD 29））的α4-整联蛋白（CD 49 d）链的mAb与针对CD 18的mAb联合使用可阻断迁移。与上述刺激相反，用IL-1α激活HUVE可抑制单核细胞响应MCP-1的跨内皮迁移。针对IL-1上调HUVE上粘附分子的mAb，即，E-选择素（CD 62 E）、细胞间粘附分子-1（CD 54）或血管细胞粘附分子-1（CD 106）不能逆转抑制作用。用IL-1α刺激的（而不是未刺激的）HUVE培养上清液处理单核细胞，可以抑制MCP-1的跨内皮迁移，但不抑制C5 a。这种上清液含有对单核细胞的趋化活性，并且针对MCP-1的mAb阻断了HUVE单层的IL-1活化的迁移抑制作用，以及来自IL-1刺激的HUVE的上清液中的趋化活性。对IL-1刺激的HUVE迁移的抑制作用对单核细胞具有特异性，因为响应于IL-8（一种相关趋化因子）的多形核白细胞跨内皮迁移不受IL-1激活HUVE的抑制。这些结果表明：（1）C5 a而非MCP-1、MIP-1 α、RANTES或PAF不仅激活单核细胞上的CD 18依赖性机制，而且激活单核细胞上的VLA-4依赖性机制，其介导穿过未刺激的HUVE的迁移;（2）IL-1（肿瘤坏死因子-α或脂多糖）激活HUVE导致有效的VLA-4（CD 494/CD 29）介导的单核细胞跨内皮迁移响应于C5 a、RANTES、MIP-1α和PAF，除了CD 18依赖性途径，但抑制对MCP-1的响应;（3）这种选择性抑制可能是由于活化的内皮细胞单层产生MCP-1，并且可能是内皮细胞响应血管外MCP-1而下调单核细胞迁移的机制之一。J. Leukoc. 58：71- 79，1995中。
We investigated the effect of interleukin‐1 (IL‐1) activation of human umbilical vein endothelium (HUVE) on human monocyte transendothelial migration induced by chemotactic factors. Monocyte migration across unacdvated endothelium in response to macrophage inflammatory protein‐lα (MIP‐1α), RANTES, platelet‐activating factor (PAF), or monocyte chemoat‐tractant protein‐1 (MCP‐1) was completely inhibited (90%) by monoclonal antibodies (mAbs; 60.3) to CD 18 of the CD11/CD18 complex on the monocyte and partially inhibited (by 75%) in response to C5a. When the HUVE was stimulated with IL‐lα (5 h, 0.1 ng/ml), monocyte migration in response to C5a, MIP‐lα, RANTES, or PAF was no longer inhibited by mAb to CD18. However, migration was blocked by the combination of mAb to the (α4‐integrin (CD49d) chain of very late antigen‐4 (CD49d(/CD29) with the mAb to CD18. In contrast to the above stimuli, activation of the HUVE with IL‐1α inhibited the transendothelial migration of monocytes in response to MCP‐1. mAbs to the adhesion molecules up‐regulated on HUVE by IL‐1, i.e., E‐selectin (CD62E), intercellular adhesion molecule‐1 (CD54) or vascular cell adhesion molecule‐1 (CD106), did not reverse the inhibitory effect. Transendothelial migration in response to MCP‐1 but not to C5a was inhibited by the treatment of monocytes with culture supernatant from IL‐1α‐stimulated (but not from unstimulated) HUVE. Such supernatant contained chemotactic activity for monocytes, and a mAb to MCP‐1 blocked the migration inhibitory effect of IL‐1 activation of the HUVE monolayer, as well as the chemotactic activity in the supernatant from IL‐1‐stimulated HUVE. The inhibitory effect on migration of IL‐1‐stimulated HUVE was specific for monocytes because polymorphonuclear leukocyte transendothelial migration in response to IL‐8 (a related chemokine) was not inhibited by IL‐1 activation of HUVE. These results demonstrate that: (1) C5a but not MCP‐1, MIP‐lα, RANTES, or PAF activates not only a CD 18‐dependent but also a VLA‐4‐dependent mechanism on monocytes, which mediates migration across unstimulated HUVE; (2) IL‐1 (tumor necrosis factor‐α or lipopolysaccharide) activation of HUVE results in efficient VLA‐4 (CD494/CD29)‐mediated monocyte transendothelial migration in response to C5a, RANTES, MIP‐1α, and PAF, in addition to the CD 18‐dependent pathway, but inhibits the response to MCP‐1; and (3) this selective inhibition is probably due to MCP‐1 production by the activated endothelium monolayer and may be one mechanism of down‐regulation by the endothelium of monocyte migration in response to extravascular MCP‐1. J. Leukoc. Biol. 58: 71–79,1995.
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影响因子：
56.9
作者：
GRAVES, DT;JIANG, YL;VALENTE, AJ
通讯作者：
VALENTE, AJ
影响因子：
56.9
作者：
HUBER, AR;KUNKEL, SL;WEISS, SJ
通讯作者：
WEISS, SJ
影响因子：
56.9
作者：
RICE, GE;BEVILACQUA, MP
通讯作者：
BEVILACQUA, MP
白细胞整合素 CD11a/CD18 和 CD11b/CD18 或细胞间粘附分子 1 的单克隆抗体可在体外抑制趋化剂刺激的中性粒细胞跨内皮迁移。
影响因子：
20.3
作者：
Furie,MB;Tancinco,MC;Smith,CW
通讯作者：
Smith,CW
人类单核细胞响应白三烯 B4 和 f-Met-Leu-Phe 跨内皮迁移的体外研究。
DOI：
--
发表时间：
1987
期刊：
The American journal of pathology
影响因子：
--
作者：
Migliorisi,G;Folkes,E;Pawlowski,N;Cramer,EB
通讯作者：
Cramer,EB