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Laser-mediated rupture of chlamydial inclusions triggers pathogen egress and host cell necrosis

Markus C Kerr1, Guillermo A Gomez1, Charles Ferguson1

  • 1Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland 4072, Australia.

Nature Communications
|March 11, 2017
PubMed

Insights

Intracellular chlamydia pathogens rupture host cell inclusions using calpains, then trigger necrotic cell death to spread. This study dissects the pathogen

Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogen-Host Interactions

Background:

  • Intracellular pathogens like chlamydia must exit host cells to infect new hosts.
  • Chlamydia egress involves breaking the inclusion (replicative niche) and host cell lysis.
  • The molecular mechanisms of chlamydial exit remain poorly understood.

Purpose of the Study:

  • To dissect the molecular events of chlamydial inclusion rupture and host cell lysis.
  • To investigate the role of host cell factors in chlamydial egress.
  • To identify the cell death pathways triggered by chlamydial exit.

Main Methods:

  • Laser ablation to selectively disrupt the chlamydial inclusion.
  • Pharmacological inhibition of host cell calpains.
  • Analysis of cell death pathways (BAK, BAX, RIP1, caspases).

Main Results:

  • Inclusion rupture is inhibited by blocking host cell calpains, but subsequent cell lysis is not affected.
  • Inclusion rupture initiates a rapid necrotic cell death pathway.
  • This pathway is independent of BAK, BAX, RIP1, and caspases.

Conclusions:

  • Chlamydial egress involves a sequential two-step process: inclusion rupture followed by host cell lysis.
  • Calpain activity is crucial for inclusion rupture.
  • The pathogen triggers a distinct necrotic cell death pathway to facilitate its release and spread.

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