Monocyte chemotactic protein-3 (MCP-3) is a C-C chemokine which interacts with the CCR1, CCR2 (MCP-1) and CCR3 receptors and has a distinct spectrum of action. The present study was designed to investigate whether human endothelial cells (EC) and, by way of comparison, monocytes express MCP-3 and its regulation by pro- and anti-inflammatory cytokines. Unstimulated human umbilical vein EC and monocytes did not express MCP-3. Bacterial lipopolysaccharides (LPS), IL-1 and TNF induced low, but appreciable levels of MCP-3 transcripts. Interferon-gamma was a much weaker, but nevertheless active, inducer. MCP-3 transcripts were considerably less abundant than those for MCP-1. IL-4, IL-13 and IL-10 did not induce MCP-3 expression. These anti-inflammatory cytokines suppressed cytokine-induced MCP-3 expression in monocytes. In contrast, IL-4, IL-13 and IL-10 either did not affect or they amplified MCP-3 induction in EC. EC-produced MCP-3 may be important in the regulation of extravasation of receptor-expressing cells, including NK cells and eosinophils.
Expression of monocyte chemotactic protein-3 in human monocytes and endothelial cells / N. Polentarutti, M. Introna, S. Sozzani, R. Mancinelli, G. Mantovani, A. Mantovani. - In: EUROPEAN CYTOKINE NETWORK. - ISSN 1148-5493. - 8:3(1997 Sep), pp. 271-274.
Expression of monocyte chemotactic protein-3 in human monocytes and endothelial cells
G. MantovaniPenultimo
;A. MantovaniUltimo
1997
Abstract
Monocyte chemotactic protein-3 (MCP-3) is a C-C chemokine which interacts with the CCR1, CCR2 (MCP-1) and CCR3 receptors and has a distinct spectrum of action. The present study was designed to investigate whether human endothelial cells (EC) and, by way of comparison, monocytes express MCP-3 and its regulation by pro- and anti-inflammatory cytokines. Unstimulated human umbilical vein EC and monocytes did not express MCP-3. Bacterial lipopolysaccharides (LPS), IL-1 and TNF induced low, but appreciable levels of MCP-3 transcripts. Interferon-gamma was a much weaker, but nevertheless active, inducer. MCP-3 transcripts were considerably less abundant than those for MCP-1. IL-4, IL-13 and IL-10 did not induce MCP-3 expression. These anti-inflammatory cytokines suppressed cytokine-induced MCP-3 expression in monocytes. In contrast, IL-4, IL-13 and IL-10 either did not affect or they amplified MCP-3 induction in EC. EC-produced MCP-3 may be important in the regulation of extravasation of receptor-expressing cells, including NK cells and eosinophils.Pubblicazioni consigliate
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