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

Anesth Analg. 2003 Nov;97(5):1312-1316. doi: 10.1213/01.ANE.0000081795.96158.3E.

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.

Implications: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anesthetics, Local / pharmacology*
  • Calcium / metabolism
  • Cell Line
  • Cell Movement / drug effects
  • Chemokine CCL2 / biosynthesis*
  • Chemotaxis, Leukocyte / drug effects*
  • DNA Primers
  • Humans
  • Inflammation / pathology*
  • Lidocaine / pharmacology*
  • Lipopolysaccharides / pharmacology
  • Monocytes / drug effects*
  • Monocytes / metabolism*
  • RNA, Messenger / biosynthesis
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / drug effects

Substances

  • Anesthetics, Local
  • Chemokine CCL2
  • DNA Primers
  • Lipopolysaccharides
  • RNA, Messenger
  • Lidocaine
  • Calcium