Staphylococcal alpha-toxin synergistically enhances inflammation caused by bacterial components

FEMS Immunol Med Microbiol. 2002 Mar 25;33(1):15-21. doi: 10.1111/j.1574-695X.2002.tb00566.x.


This study was performed to investigate the in vivo effects of staphylococcal alpha-toxin on phagocytosis and the secretion of proinflammatory cytokines at local sites of intraperitoneal toxin-challenged mice. A dosage of 45 hemolytic units (HU) of alpha-toxin induced a marked increase in the peritoneal neutrophil count. The toxin caused a 52% decrease in phagocytosis by peritoneal macrophages, compared with that of control mice receiving Staphylococcus aureus particles alone. However, no effect on phagocytosis in neutrophils was observed. A dosage of 45 HU toxin and the synergistic activity of S. aureus particles strongly induced interleukin (IL) 6 secretion but only mildly induced IL-1alpha secretion. The toxin did not induce the secretion of tumor necrosis factor-alpha (TNF-alpha). Interestingly, S. aureus culture supernatant induced the secretion of TNF-alpha in cultured macrophages. These results suggest that alpha-toxin damages the primary host defense system by inducing the oversecretion of IL-1alpha and IL-6, but not TNF-alpha, via a mechanism that requires the synergistic action of bacterial components.

MeSH terms

  • Animals
  • Bacterial Toxins / toxicity*
  • Cells, Cultured
  • Drug Synergism
  • Hemolysin Proteins / toxicity*
  • Interleukin-1 / metabolism
  • Interleukin-6 / metabolism
  • Macrophage Activation
  • Macrophages, Peritoneal / metabolism
  • Macrophages, Peritoneal / pathology
  • Male
  • Mice
  • Neutrophils / pathology
  • Peritonitis / chemically induced*
  • Peritonitis / pathology
  • Phagocytosis
  • Staphylococcus aureus / immunology
  • Tumor Necrosis Factor-alpha / metabolism


  • Bacterial Toxins
  • Hemolysin Proteins
  • Interleukin-1
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • staphylococcal alpha-toxin