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Recruitment of BAD by the Chlamydia trachomatis vacuole correlates with host-cell survival

Philippe Verbeke1, Lynn Welter-Stahl, Songmin Ying

  • 1Institut Jacques Monod, Université Paris-Denis Diderot, Paris, France.

Plos Pathogens
|May 20, 2006
PubMed

Insights

Chlamydia trachomatis infection protects host cells from apoptosis by sequestering the pro-apoptotic protein BAD. This mechanism involves a bacterial inclusion protein interacting with host cell factor 14-3-3beta, facilitated by the PI3K/AKT pathway.

Area of Science:

  • Cell Biology
  • Microbiology
  • Immunology

Background:

  • Chlamydiae are obligate intracellular bacteria that reside within a vacuole called an inclusion.
  • Chlamydia-infected cells exhibit resistance to mitochondrion-dependent apoptosis, partly through the degradation of BH3-only proteins.
  • The host cell protein 14-3-3beta interacts with apoptotic signaling pathways in a phosphorylation-dependent manner.

Purpose of the Study:

  • To investigate the role of the phosphatidylinositol-3 kinase (PI3K) pathway in the resistance of Chlamydia-infected cells to apoptosis.
  • To elucidate the mechanism by which Chlamydia trachomatis protects host cells from apoptosis, focusing on the interaction between bacterial and host factors.

Main Methods:

  • Inhibition of the PI3K pathway using specific inhibitors.
  • Assessment of apoptosis induction by staurosporine and measurement of mitochondrial cytochrome c release.
  • Co-localization studies of 14-3-3beta with the Chlamydia inclusion.
  • Analysis of AKT/protein kinase B activation and BAD protein phosphorylation status.
  • Short-interfering RNA-mediated depletion of AKT.
  • Comparison of Chlamydia trachomatis, Chlamydia pneumoniae, and Chlamydia muridarum infection models.

Main Results:

  • Inhibition of PI3K in C. trachomatis-infected cells restored sensitivity to apoptosis and induced mitochondrial cytochrome c release.
  • 14-3-3beta co-localized with the C. trachomatis inclusion via interaction with a bacterial inclusion membrane protein.
  • The PI3K/AKT pathway in C. trachomatis-infected cells maintained BAD protein in a phosphorylated state, sequestering it to the inclusion via 14-3-3beta.
  • PI3K inhibition or AKT depletion reversed apoptosis resistance, leading to BAD release and mitochondrial apoptosis.
  • These protective mechanisms were not observed in C. pneumoniae or C. muridarum infections.

Conclusions:

  • Chlamydia trachomatis utilizes the host PI3K/AKT pathway to phosphorylate and sequester the pro-apoptotic protein BAD via interaction with 14-3-3beta at the inclusion.
  • This sequestration of BAD away from mitochondria is a key mechanism by which C. trachomatis protects infected host cells from apoptosis.
  • The observed host-cell protection mechanism is specific to C. trachomatis and not shared by other Chlamydia species like C. pneumoniae or C. muridarum.

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