C-jun N-terminal kinase-mediated signaling is essential for Staphylococcus aureus-induced U937 apoptosis

Jia-he Wang1, Bo Yu, Hui-yan Niu

  • 1Department of Geriatrics, Shengjing Hospital, China Medical University, Shenyang 110004, China. cmuwjh@126.com

Abstract

Insights

Staphylococcus aureus (S. aureus) triggers U937 cell death via JNK signaling. SP600125, a JNK inhibitor, effectively prevents S. aureus-induced apoptosis in these cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Staphylococcus aureus (S. aureus) is a pathogen that can induce cell death.
  • U937 cells are a human monocytic cell line susceptible to S. aureus infection.
  • The c-jun N-terminal protein kinase (JNK) pathway is implicated in cellular stress responses and apoptosis.

Purpose of the Study:

  • To investigate the role of JNK signaling in S. aureus-induced U937 cell death.
  • To determine if SP600125, a JNK inhibitor, can protect U937 cells from S. aureus-induced apoptosis.

Main Methods:

  • U937 cells were treated with S. aureus with or without SP600125.
  • Apoptosis was assessed using flow cytometry.
  • JNK, Bax, and caspase-3 activities were measured via Western blotting.

Main Results:

  • S. aureus induced apoptosis in U937 cells in a time-dependent manner.
  • Expression of phospho-JNK and Bax, and activity of caspase-3, increased following S. aureus treatment.
  • SP600125 significantly reduced S. aureus-induced apoptosis.

Conclusions:

  • S. aureus induces U937 cell apoptosis through JNK phosphorylation and activation of Bax and caspase-3.
  • SP600125 protects U937 cells from S. aureus-induced apoptosis by inhibiting JNK activity.

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