Erythromycin Inhibition of Lipopolysaccharide-Stimulated Tumor Necrosis Factor Alpha Production by Human Monocytes in Vitro

Ann Otol Rhinol Laryngol Suppl. 1992 Oct;157:16-20. doi: 10.1177/0003489492101s1005.

Abstract

The mechanism of clinical effectiveness of low-dose and long-term erythromycin (EM) treatment for diffuse panbronchiolitis, sinobronchial syndrome, and associated otitis media with effusion was investigated by studying the effects of EM on tumor necrosis factor alpha (TNF-alpha) production by cultured human monocytes stimulated with lipopolysaccharide. At concentrations of 0.1 microgram/mL or more, EM inhibited TNF-alpha release from human monocytes stimulated by lipopolysaccharide in a dose-dependent manner. Of the other macrolides tested, roxithromycin, an EM derivative, also showed significant inhibition of TNF-alpha production, whereas josamycin failed to inhibit TNF-alpha release from monocytes. Nonmacrolidic drugs such as minocycline hydrochloride, ofloxacin, or penicillin G had no significant effect on TNF-alpha production. These results suggest that the clinical improvement of chronic respiratory diseases by EM may depend on the suppression of production of inflammatory cytokines such as TNF-alpha.

MeSH terms

  • Anti-Bacterial Agents / pharmacology
  • Erythromycin / pharmacology*
  • Escherichia coli
  • Humans
  • In Vitro Techniques
  • Lipopolysaccharides / pharmacology*
  • Monocytes / drug effects
  • Monocytes / metabolism*
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • Anti-Bacterial Agents
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Erythromycin