Mechanisms of Staphylococcus aureus induced apoptosis of human endothelial cells

Apoptosis. 2001 Dec;6(6):431-9. doi: 10.1023/a:1012445925628.

Abstract

Staphylococcus aureus plays an important role in sepsis, pneumonia and wound infections. Here, we demonstrate that infection with several S. aureus strains results in apoptosis of human endothelial cells. S. aureus induced an activation of cellular caspases, the acid sphingomyelinase, a release of cytochrome c and a stimulation of Jun NH2-terminal kinase (JNK). The significance of these findings is indicated by a prevention of S. aureus triggered apoptosis of human cells deficient for ASM or upon genetic or pharmacological inhibition of JNK or caspases, respectively.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Apoptosis*
  • Caspases / metabolism
  • Cell Line
  • Cells, Cultured
  • Cytochrome c Group / metabolism
  • DNA Fragmentation
  • Endothelium / cytology*
  • Endothelium / microbiology
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / microbiology
  • Enzyme Activation
  • Flow Cytometry
  • Humans
  • JNK Mitogen-Activated Protein Kinases*
  • MAP Kinase Kinase 4
  • Mitochondria / metabolism
  • Mitogen-Activated Protein Kinase Kinases / metabolism
  • Sphingomyelin Phosphodiesterase / deficiency
  • Sphingomyelin Phosphodiesterase / metabolism
  • Staphylococcus aureus / metabolism*
  • Time Factors
  • Transfection
  • Umbilical Veins / cytology
  • Umbilical Veins / microbiology

Substances

  • Cytochrome c Group
  • JNK Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase 4
  • Mitogen-Activated Protein Kinase Kinases
  • Sphingomyelin Phosphodiesterase
  • Caspases