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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Staphylococcus aureus induces apoptosis of human monocytic U937 cells via NF-kappaB signaling pathways

Jia He Wang1, Yi Jun Zhou, Ping He

  • 1Department of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, PR China. wangjh1@sj-hospital.org

Microbial Pathogenesis
|July 6, 2010
PubMed

Insights

Staphylococcus aureus infection triggers apoptosis in monocytes by inhibiting nuclear transcription factor-kappaB (NF-kappaB). This leads to reduced anti-apoptotic proteins and increased caspase-3 activity, revealing a key cell death pathway.

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Staphylococcus aureus is a significant opportunistic pathogen causing various infections.
  • S. aureus is known to induce apoptosis in diverse cell types.
  • Mechanisms of S. aureus-induced cell death in primary monocytes and U937 cells remain unclear.

Purpose of the Study:

  • To elucidate the mechanisms of S. aureus-induced cell death in primary monocytes and U937 cells.
  • To investigate the role of nuclear transcription factor-kappaB (NF-kappaB) in this process.
  • To identify key apoptotic pathways involved.

Main Methods:

  • Infection of primary monocytes and U937 cells with S. aureus.
  • Analysis of cell death using apoptosis assays.
  • Assessment of NF-kappaB expression and activity.
  • Quantification of anti-apoptotic and pro-apoptotic gene/protein expression (Bcl-2, survivin, cIAP, XIAP, Bax, caspase-3).
  • Measurement of caspase-3 activity.

Main Results:

  • S. aureus infection induced rapid, dose- and time-dependent apoptosis in monocytes and U937 cells.
  • Apoptosis correlated with reduced NF-kappaB expression.
  • S. aureus inhibited NF-kappaB, leading to decreased levels of NF-kappaB-regulated anti-apoptotic proteins (Bcl-2, survivin, cIAP, XIAP).
  • S. aureus upregulated pro-apoptotic genes (Bax, caspase-3) and increased caspase-3 activity.

Conclusions:

  • S. aureus infection induces apoptosis in primary monocytes and U937 cells via a caspase-dependent inhibition of NF-kappaB.
  • This pathway involves the downregulation of anti-apoptotic proteins and upregulation of pro-apoptotic factors.
  • Understanding this mechanism is crucial for developing therapeutic strategies against S. aureus infections.

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