Trichomonas vaginalis-induced apoptosis in RAW264.7 cells is regulated through Bcl-xL, but not Bcl-2

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J-H Chang1, Y-S Ryang, S-K Kim

  • 1Department of Biomedical Laboratory Science, College of Health Science, Yonsei University, Wonju, South Korea.

Parasite Immunology
|July 29, 2004
PubMed

Insights

Trichomonas vaginalis induces apoptosis in RAW264.7 cells through a Bcl-x(L)-dependent pathway. Overexpressed Bcl-x(L) inhibits this cell death, while Bcl-2 has no effect.

Area of Science:

  • Immunology
  • Cell Biology
  • Parasitology

Background:

  • The Bcl-2 family of proteins regulates apoptosis.
  • RAW264.7 cells are a murine macrophage cell line susceptible to infection.
  • Trichomonas vaginalis is a protozoan parasite that can infect host cells.

Purpose of the Study:

  • To investigate the role of anti-apoptotic proteins Bcl-2 and Bcl-x(L) in T. vaginalis-induced apoptosis in RAW264.7 cells.
  • To determine the mechanism of T. vaginalis-induced cell death.

Main Methods:

  • RAW264.7 cells were treated with T. vaginalis.
  • Expression levels of Bcl-2 and Bcl-x(L) were analyzed.
  • Mitochondrial membrane potential, cytochrome c release, caspase activation, and PARP cleavage were assessed.
  • Cells were transfected with overexpressed Bcl-x(L) or treated with caspase inhibitors.

Main Results:

  • Bcl-2 expression remained unchanged and did not prevent apoptosis.
  • T. vaginalis treatment decreased Bcl-x(L) expression and increased Bax activation.
  • Overexpression of Bcl-x(L) inhibited T. vaginalis-induced apoptosis, cytochrome c release, caspase-9 cleavage, and PARP cleavage.
  • Caspase inhibitors blocked T. vaginalis-induced down-regulation of Bcl-x(L), indicating caspase-3's role.

Conclusions:

  • T. vaginalis induces apoptosis in RAW264.7 cells via a Bcl-x(L)-dependent mechanism.
  • Bcl-x(L) plays a critical role in regulating T. vaginalis-induced apoptosis.
  • Caspase-3 is involved in the down-regulation of Bcl-x(L) during T. vaginalis infection.

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