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Am J Physiol Heart Circ Physiol 283: H2584-H2591, 2002. First published August 29, 2002; doi:10.1152/ajpheart.00349.2002
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Vol. 283, Issue 6, H2584-H2591, December 2002

Role of endothelial MCP-1 in monocyte adhesion to inflamed human endothelium under physiological flow

U. Maus1, S. Henning1, H. Wenschuh2, K. Mayer1, W. Seeger1, and J. Lohmeyer1

1 Department of Internal Medicine, Justus-Liebig University, Giessen 35392; and 2 Jerini AG, 10115 Berlin, Germany

Monocyte chemoattractant protein-1 (MCP-1) is an essential chemokine involved in monocyte traffic across endo- and epithelial barriers both in vitro and in vivo. However, the contribution of endothelial MCP-1 signaling via its CCR2 receptor in monocyte adhesion to inflamed endothelium under flow is incompletely understood. A sensitive flow chamber assay was used to assess monocyte adhesion to TNF-alpha -activated primary human pulmonary artery endothelial cells (HPAEC) during physiological shear stress. Monocyte adhesion was markedly reduced (~45%) when HPAEC-derived MCP-1 was either neutralized with anti-MCP-1 mAb or inhibited by translational arrest of MCP-1 mRNA transcripts with MCP-1 antisense oligomers. Corresponding efficacy was observed for blockade of monocyte CCR2 receptor function by anti-CCR2 mAb or MCP-1 antagonists (9-76 analog). The impact of endothelial MCP-1 on monocyte-HPAEC adhesion occurred via beta 2-integrin but not via beta 1-integrin adhesion pathways. In this line, pretreatment of monocytes with MCP-1 but not RANTES provoked a rapid and transient neoepitope 24 expression on beta 2-integrin alpha -chains, as analyzed by increased reporter mAb24 binding. Collectively, our data show an important cross talk of endothelial MCP-1 with monocyte CCR2 effecting monocyte firm adhesion to inflamed HPAEC under physiological flow conditions.

monocytes/macrophages; adhesion molecules; chemokines; cell trafficking; monocyte chemoattractant protein-1


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