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IAP-IAP complexes required for apoptosis resistance of C. trachomatis-infected cells

Krishnaraj Rajalingam1, Manu Sharma, Nicole Paland

  • 1Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.

Plos Pathogens
|October 31, 2006
PubMed

Insights

Chlamydia trachomatis infection prevents cell death by up-regulating cellular inhibitor of apoptosis (cIAP)-2. Inhibitor of apoptosis proteins (IAPs) function as stable complexes, a novel mechanism for apoptosis resistance.

Area of Science:

  • Cell Biology
  • Immunology
  • Microbiology

Background:

  • Host cells infected with Chlamydia trachomatis exhibit remarkable resistance to apoptosis.
  • The precise molecular mechanisms behind this apoptosis resistance in infected cells remain largely unelucidated.

Purpose of the Study:

  • To investigate the molecular mechanisms by which apoptosis, induced by tumor necrosis factor (TNF) receptor signaling, is inhibited in Chlamydia trachomatis-infected epithelial cells.

Main Methods:

  • Investigated the role of cellular inhibitor of apoptosis (cIAP) proteins in apoptosis resistance.
  • Utilized small interfering RNA (siRNA) to modulate cIAP expression and assess its impact on TNF-induced apoptosis.
  • Analyzed the formation and stability of heteromeric complexes of inhibitor of apoptosis proteins (IAPs).

Main Results:

  • Chlamydia trachomatis infection up-regulates cIAP-2, contributing to apoptosis resistance.
  • Interference with cIAP-2 up-regulation sensitized infected cells to TNF-induced apoptosis.
  • cIAP-1, cIAP-2, and X-linked IAP are essential for maintaining apoptosis resistance, functioning as stable heteromeric complexes.
  • The stability of cIAP-2 is modulated by X-linked IAP, with their interaction enhanced in infected cells.

Conclusions:

  • Inhibitor of apoptosis proteins (IAPs) maintain apoptosis resistance in Chlamydia trachomatis-infected cells through stable heteromeric complex formation.
  • This heteromeric complex formation represents a novel regulatory mechanism for IAPs and their role in modulating apoptosis.

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