Grepafloxacin inhibits tumor necrosis factor-alpha-induced interleukin-8 expression in human airway epithelial cells

Life Sci. 2000;66(5):PL 77-82. doi: 10.1016/s0024-3205(99)00614-1.

Abstract

We examined the effect of grepafloxacin (GPFX), a new fluoroquinolone antimicrobial agent, on interleukin-8 (IL-8) expression in tumor necrosis factor-alpha (TNF-alpha)-stimulated human airway epithelial cells (AEC). GPFX inhibited IL-8 protein production as well as mRNA expression in a concentration-dependent manner (2.5 - 25 micro g/ml), but the inhibition of IL-8 expression by corresponding concentrations of GPFX to serum and airway lining fluids was not complete. We discuss the modulatory effect of GPFX on IL-8 production in the context of its efficacy on controlling chronic airway inflammatory diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Infective Agents / pharmacology*
  • Cell Survival / drug effects
  • Cells, Cultured
  • Culture Media, Conditioned / chemistry
  • Dose-Response Relationship, Drug
  • Fluoroquinolones*
  • Humans
  • Interleukin-8 / biosynthesis*
  • Interleukin-8 / genetics
  • Piperazines / pharmacology*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Respiratory Mucosa / cytology
  • Respiratory Mucosa / drug effects*
  • Respiratory Mucosa / metabolism*
  • Time Factors
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Up-Regulation / drug effects

Substances

  • Anti-Infective Agents
  • Culture Media, Conditioned
  • Fluoroquinolones
  • Interleukin-8
  • Piperazines
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • grepafloxacin