Inhibitory effects of erythromycin on wear debris-induced VEGF/Flt-1 gene production and osteolysis

Inflamm Res. 2009 Jul;58(7):413-21. doi: 10.1007/s00011-009-0007-9. Epub 2009 Mar 5.

Abstract

Objectives: A highly vascularized and inflammatory periprosthetic tissue augments the progress of aseptic loosening, a major clinical problem after total joint replacement. The purpose of this study is to investigate the effect of erythromycin (EM) on ultra high molecular weight polyethylene (UHMWPE) particle-induced VEGF/VEGF receptor 1 (Flt-1) gene production and inflammatory osteolysis in a mouse model.

Methods: UHMWPE particles were introduced into established air pouches on BALB/c mice, followed by implantation of calvaria bone from syngeneic littermates. EM treatment started 2 weeks after bone implantation (5 mg/kg day, i.p. injection). Mice without drug treatment as well as mice injected with saline alone were included. Pouch tissues were harvested 2 weeks after bone implantation. Expression of VEGF, Flt-1, RANKL, IL-1, TNF and CD68 was measured by immunostain and RT-PCR, and implanted bone resorption was analyzed by micro-CT (muCT).

Results: Exposure to UHMWPE induced pouch tissue inflammation, increase of VEGF/Flt-1 proteins, and increased bone resorption. EM treatment significantly improved UHMWPE particle-induced tissue inflammation, reduced VEGF/Flt-1 protein expression, and diminished the number of TRAP(+) cells, as well as the implanted bone resorption.

Conclusion: This study demonstrated that EM inhibited VEGF and Flt-1 gene expression. The molecular mechanism of EM action on VEGF/Flt-1 signaling-mediated osteoclastogenesis warrants further investigation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Anti-Inflammatory Agents / therapeutic use
  • Disease Models, Animal
  • Erythromycin / pharmacology*
  • Erythromycin / therapeutic use
  • Female
  • Gene Expression Regulation / drug effects*
  • Interleukin-1 / immunology
  • Mice
  • Mice, Inbred BALB C
  • Osteolysis / chemically induced
  • Osteolysis / drug therapy
  • Osteolysis / genetics*
  • Osteolysis / immunology
  • Polyethylenes
  • RANK Ligand / immunology
  • Sodium Chloride
  • Tumor Necrosis Factor-alpha / immunology
  • Vascular Endothelial Growth Factor A / genetics*
  • Vascular Endothelial Growth Factor A / immunology
  • Vascular Endothelial Growth Factor Receptor-1 / genetics*
  • Vascular Endothelial Growth Factor Receptor-1 / immunology

Substances

  • Anti-Inflammatory Agents
  • Interleukin-1
  • Polyethylenes
  • RANK Ligand
  • Tnfsf11 protein, mouse
  • Tumor Necrosis Factor-alpha
  • Vascular Endothelial Growth Factor A
  • ultra-high molecular weight polyethylene
  • vascular endothelial growth factor A, mouse
  • Sodium Chloride
  • Erythromycin
  • Flt1 protein, mouse
  • Vascular Endothelial Growth Factor Receptor-1