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Host cell Golgi anti-apoptotic protein (GAAP) and growth of Chlamydia pneumoniae

Eveliina Markkula1, Jaakko Hulkkonen, Tuula Penttilä

  • 1Haartman Institute, Department of Virology, PO Box 21, University of Helsinki, FI-00014 Helsinki, Finland.

Microbial Pathogenesis
|September 25, 2012
PubMed

Insights

Chlamydia pneumoniae protein CPn0809 interacts with host Golgi anti-apoptotic protein (GAAP). This interaction modulates bacterial growth within host cells, impacting infection pathogenesis.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Chlamydia pneumoniae is an important human pathogen.
  • The function of C. pneumoniae protein CPn0809 in infection is unknown.
  • CPn0809 is a substrate of the type III secretion system.

Purpose of the Study:

  • To identify host cell interaction partners of CPn0809.
  • To investigate the role of CPn0809-host interactions in C. pneumoniae infection.

Main Methods:

  • Yeast two-hybrid screening to identify interacting proteins.
  • Transfection studies to confirm interactions.
  • siRNA-mediated gene silencing to assess protein function.
  • Quantitative PCR and inclusion counts to measure bacterial load.

Main Results:

  • Golgi anti-apoptotic protein (GAAP) was identified as a potential interaction partner of CPn0809.
  • GAAP expression remained stable during C. pneumoniae infection.
  • Knock-down of GAAP increased C. pneumoniae genome numbers and bacterial growth.
  • GAAP silencing did not affect host cell apoptosis susceptibility.

Conclusions:

  • CPn0809 interacts with host GAAP.
  • The C. pneumoniae-GAAP interaction modulates bacterial growth within host cells.
  • This interaction plays a role in C. pneumoniae infection pathogenesis.

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