Dobutamine inhibits monocyte chemoattractant protein-1 production and chemotaxis in human monocytes.

Abstract

It has been reported that, in patients with acute myocardial infarction or congestive heart failure, monocyte chemoattractant protein-1 (MCP-1) plays an important role in the development of inflammatory responses and that the level of MCP-1 is correlated with the severity of the disease. We conducted this study to investigate the effects of dobutamine and dopamine on lipopolysaccharide (LPS)-induced MCP-1 production in human monocytic THP-1 cells. Monocytes were incubated in vitro with LPS for 16 h at 37 degrees C in the presence or absence of dobutamine or dopamine. Enzyme-linked immunosorbent assay was used to examine the effect of dobutamine on MCP-1 synthesis, with the MCP-1 messenger RNA expression examined by reverse transcriptase-polymerase chain reaction. Dobutamine inhibited LPS-induced production of MCP-1, as well as messenger RNA expression, in a dose-dependent manner, whereas dopamine had no significant effect. Furthermore, we demonstrated that dobutamine suppressed MCP-1-induced chemotaxis and peak [Ca(2+)](i) in monocytic THP-1 cells. These findings suggest that dobutamine may modulate monocyte activation, such as chemotaxis and [Ca(2+)](i), as well as MCP-1 production, during therapy for congestive heart failure. Monocyte chemoattractant protein-1 (MCP-1) plays important roles in the inflammatory processes associated with pathogenesis of cardiovascular diseases. In this study, dobutamine was found to inhibit lipopolysaccharide-induced MCP-1 production and messenger RNA expression, as well as MCP-1-induced chemotaxis and peak [Ca(2+)](i), in human monocytes.