IL-1 activation of endothelium supports VLA-4 (CD49d/CD29)-mediated monocyte transendothelial migration to C5a, MIP-1 alpha, RANTES, and PAF but inhibits migration to MCP-1: a regulatory role for endothelium-derived MCP-1.

摘要: We investigated the effect of interleukin-1 (IL-1) activation human umbilical vein endothelium (HUVE) on monocyte transendothelial migration induced by chemotactic factors. Monocyte across unactivated in response to macrophage inflammatory protein-1 alpha (MIP-1 alpha), RANTES, platelet-activating factor (PAF), or chemoattractant (MCP-1) was completely inhibited (90%) monoclonal antibodies (mAbs; 60.3) CD18 CD11/CD18 complex and partially (by 75%) C5a. When HUVE stimulated with IL-1 (5 h, 0.1 ng/ml), C5a, MIP-1 alpha, PAF no longer mAb CD18. However, blocked combination 4-integrin (CD49d) chain very late antigen-4 (CD49d/CD29) In contrast above stimuli, monocytes MCP-1. mAbs adhesion molecules up-regulated IL-1, i.e., E-selectin (CD62E), intercellular molecule-1 (CD54) vascular cell (CD106), did not reverse inhibitory effect. Transendothelial MCP-1 but C5a treatment culture supernatant from alpha-stimulated (but unstimulated) HUVE. Such contained activity for monocytes, a monolayer, as well IL-1-stimulated The specific because polymorphonuclear leukocyte IL-8 (a related chemokine) HUVE.(ABSTRACT TRUNCATED AT 250 WORDS)