Recruitment of BAD by the Chlamydia trachomatis Vacuole Correlates with Host-Cell Survival
2006

How Chlamydia trachomatis Helps Infected Cells Survive

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Author Information

Author(s): Philippe Verbeke, Lynn Welter-Stahl, Ying Songmin, Jon Hansen, Georg Häcker, Toni Darville, David M. Ojcius

Primary Institution: Institut Jacques Monod, Université Paris—Denis Diderot, Paris, France

Hypothesis

Does the phosphatidylinositol-3 kinase (PI3K) pathway contribute to the resistance of Chlamydia trachomatis-infected cells to apoptosis?

Conclusion

Chlamydia trachomatis infection activates the PI3K pathway, which helps infected cells avoid apoptosis by sequestering the pro-apoptotic protein BAD.

Supporting Evidence

  • Inhibition of PI3K made Chlamydia-infected cells sensitive to apoptosis.
  • More than 95% of Chlamydia-infected cells were resistant to staurosporine-induced apoptosis.
  • Phosphorylated BAD was sequestered away from mitochondria in infected cells.

Takeaway

Chlamydia trachomatis can trick our cells into staying alive longer by using a special pathway that stops them from dying, even when they should.

Methodology

The study involved infecting HeLa cells with Chlamydia trachomatis and treating them with staurosporine to induce apoptosis, while assessing the role of the PI3K pathway and BAD phosphorylation.

Limitations

The study primarily focused on one strain of Chlamydia and may not generalize to all strains or other pathogens.

Participant Demographics

HeLa cells, a human epithelial cell line.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.ppat.0020045

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