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The Chlamydia trachomatis Inclusion Membrane Protein CpoS Counteracts STING-Mediated Cellular Surveillance and

Barbara S Sixt1, Robert J Bastidas2, Ryan Finethy2

  • 1Department of Molecular Genetics and Microbiology, Duke University, Durham, NC 27710, USA; INSERM U1138, Centre de Recherche des Cordeliers, Paris 75006, France; Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris 75006, France; Université Paris Descartes, Paris 75006, France; Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif 94800, France.

Cell Host & Microbe
|January 3, 2017
PubMed

Insights

Chlamydia uses the CpoS protein to prevent host cell death, which is essential for its survival. CpoS deficiency triggers cell death pathways involving STING, impacting Chlamydia pathogenesis.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Chlamydia evades host cell death to establish a replicative niche.
  • Mechanisms by which Chlamydia inhibits cell death are largely unknown.

Purpose of the Study:

  • To identify Chlamydia factors that modulate host cell death.
  • To elucidate the role of CpoS in Chlamydia-induced cell death and host immune response.

Main Methods:

  • Screening of a Chlamydia mutant library for cell death modulators.
  • Investigating the impact of CpoS inactivation on host cell death pathways (apoptosis, necrosis).
  • Analyzing host immune responses, including the cGAS/STING/TBK1/IRF3 pathway, in CpoS-deficient infections.

Main Results:

  • Inactivation of inclusion membrane protein CpoS (Chlamydia promoter of survival) induced rapid host cell death.
  • CpoS-mediated protection is spatially restricted to the Chlamydia inclusion.
  • CpoS-deficient Chlamydia exacerbated type I interferon response via cGAS/STING/TBK1/IRF3.
  • STING disruption, but not cGAS or IRF3, attenuated Chlamydia-induced cell death.

Conclusions:

  • CpoS is a critical Chlamydia factor that prevents host cell death.
  • STING mediates Chlamydia-induced cell death independently of interferon regulation.
  • CpoS is essential for Chlamydia pathogenesis and in vivo propagation.

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