Lidocaine attenuates monocyte chemoattractant protein-1 production and chemotaxis in human monocytes: possible mechanisms for its effect on inflammation.

Abstract

The recruitment and activation of peripheral blood monocytes are potentially critical regulatory events for the control of inflammation. Increased levels of monocyte chemoattractant protein (MCP)-1 have been reported in several inflammatory disorders. In this study, we examined the effect of lidocaine on lipopolysaccharide-stimulated MCP-1 secretion and MCP-1 induced chemotaxis in a human monocytic cell line, THP-1. Lidocaine inhibited lipopolysaccharide-induced MCP-1 production as well as messenger RNA expression in a dose-dependent manner. Furthermore, we demonstrated that lidocaine suppressed MCP-1-induced chemotaxis and peak cytosolic-free calcium in THP-1 cells. These results suggest that lidocaine may modulate MCP-1 production and MCP-1-induced activation in inflammatory cells. Monocyte chemoattractant protein-1 (MCP-1) plays important roles in the inflammatory processes. Lidocaine may modulate MCP-1-induced monocyte response, as reflected by chemotaxis, cytosolic-free calcium, and lipopolysaccharide-induced MCP-1 production by human monocytic THP-1 cells.