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Endoplasmic reticulum stress response is involved in Mycobacterium tuberculosis protein ESAT-6-mediated apoptosis

Hong-Hee Choi1, Dong-Min Shin, Gun Kang

  • 1Department of Microbiology, College of Medicine, Chungnam National University, Daejeon, South Korea.

FEBS Letters
|April 27, 2010
PubMed

Insights

The tuberculosis bacterium

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Mycobacterium tuberculosis (Mtb) infection triggers apoptosis for bacterial clearance.
  • The Mtb antigen ESAT-6 induces apoptosis in human macrophages and epithelial cells.

Purpose of the Study:

  • To investigate the mechanism by which ESAT-6 induces apoptosis in human epithelial cells.
  • To explore the role of endoplasmic reticulum (ER) stress in ESAT-6-mediated apoptosis.

Main Methods:

  • Stimulation of A549 human epithelial cells with ESAT-6.
  • Measurement of intracellular Ca(2+) concentration.
  • Assessment of reactive oxygen species (ROS) accumulation.
  • Analysis of ER stress markers and apoptosis induction.

Main Results:

  • ESAT-6 treatment induced ER stress in A549 cells.
  • ESAT-6 increased intracellular Ca(2+) levels, leading to ROS accumulation.
  • ROS accumulation triggered ER stress-induced apoptosis.
  • A novel apoptotic pathway mediated by ESAT-6 via ER stress was identified.

Conclusions:

  • ESAT-6 induces apoptosis in epithelial cells through ER stress.
  • The pathway involves increased intracellular Ca(2+) and ROS accumulation.
  • This finding reveals a new mechanism of Mtb pathogenesis in tuberculosis.

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