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The chlamydial inclusion preferentially intercepts basolaterally directed sphingomyelin-containing exocytic vacuoles

Elizabeth R Moore1, Elizabeth R Fischer, David J Mead

  • 1Host-Parasite Interactions Section, Laboratory of Intracellular Parasites, National Institute of Allergy and Infectious Diseases, Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840, USA.

Traffic (Copenhagen, Denmark)
|September 10, 2008
PubMed

Insights

Chlamydia trachomatis infection disrupts host cell lipid trafficking, specifically retaining sphingomyelin (SM) within the bacterial inclusion. This suggests the pathogen preferentially intercepts SM-containing vesicles, altering cellular lipid distribution.

Area of Science:

  • Microbiology
  • Cell Biology
  • Biochemistry

Background:

  • Chlamydiae are obligate intracellular bacteria that reside within a specialized vacuole, the inclusion.
  • The inclusion evades host cell degradation pathways by intercepting specific Golgi-derived vesicles.
  • Sphingomyelin (SM) and cholesterol are key lipids found in these intercepted vesicles.

Purpose of the Study:

  • To investigate the specific lipid trafficking alterations caused by Chlamydia trachomatis infection.
  • To determine if the chlamydial inclusion preferentially targets sphingomyelin (SM) or glucosylceramide (GlcCer).
  • To develop and utilize a polarized epithelial cell model for studying vectoral lipid transport.

Main Methods:

  • Development of a polarized epithelial cell model using C2BBe1 cells.
  • Infection of polarized cells with Chlamydia trachomatis (L2 strain).
  • Tracking of fluorescently labeled lipids (NBD-ceramide, NBD-GlcCer, NBD-SM) and analysis of their cellular distribution.

Main Results:

  • Polarized C2BBe1 cells supported Chlamydia trachomatis infection and maintained polarization.
  • Chlamydia trachomatis infection led to the retention of sphingomyelin (SM) within infected cells.
  • A disruption of basolateral SM trafficking was observed, while glucosylceramide (GlcCer) trafficking remained unaffected.
  • Purified Chlamydia trachomatis retained only SM, not GlcCer.
  • Infection with Coxiella burnetii did not alter polarized lipid trafficking, indicating a Chlamydia-specific effect.

Conclusions:

  • The chlamydial inclusion preferentially intercepts basolaterally-directed sphingomyelin (SM)-containing exocytic vesicles.
  • This interception leads to a divergence in the trafficking pathways of SM and GlcCer.
  • The observed lipid retention is a specific mechanism employed by Chlamydia trachomatis during infection.

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