Fosfomycin inhibits NF-kappaB activation in U-937 and Jurkat cells

Int J Antimicrob Agents. 2003 Jun;21(6):589-92. doi: 10.1016/s0924-8579(03)00054-2.

Abstract

Fosfomycin exerts anti-inflammatory effects through inhibiting the production of proinflammatory cytokines. Transcription of the genes for these proinflammatory cytokines is regulated by NF-kappaB. We tested the hypothesis that fosfomycin inhibits the activation of NF-kappaB induced by tumor necrosis factor-alpha (TNF-alpha) in human monocytic U-937 cells, and a T cell line (Jurkat). Western blot analysis demonstrated that fosfomycin inhibits NF-kappaB activation in both cells. Flow cytometry revealed that fosfomycin suppresses NF-kappaB activation in both cells in a dose-related manner. These findings are consistent with the idea that fosfomycin suppresses the production of proinflammatory cytokines via inhibition of NF-kappaB activation.

MeSH terms

  • Anti-Bacterial Agents / pharmacology
  • Blotting, Western
  • Dose-Response Relationship, Drug
  • Flow Cytometry
  • Fosfomycin / pharmacology*
  • Gene Expression Regulation / drug effects*
  • Humans
  • Jurkat Cells
  • NF-kappa B / genetics*
  • NF-kappa B / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology
  • U937 Cells

Substances

  • Anti-Bacterial Agents
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Fosfomycin