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Characterization of Chlamydia pneumoniae persistence in HEp-2 cells treated with gamma interferon

L G Pantoja1, R D Miller, J A Ramirez

  • 1Division of Infectious Diseases, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40292, USA.

Infection and Immunity
|November 14, 2001
PubMed

Insights

Gamma interferon (IFN-gamma) limits Chlamydia pneumoniae persistence by reducing replication and altering inclusion bodies. This suggests a mechanism for controlling C. pneumoniae infection and its link to atherosclerosis.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Chlamydia pneumoniae infection is linked to atherosclerosis.
  • Understanding C. pneumoniae persistence mechanisms is crucial.

Purpose of the Study:

  • To investigate the impact of gamma interferon (IFN-gamma)-mediated indoleamine 2,3-dioxygenase activity on C. pneumoniae.
  • To analyze effects on bacterial persistence, inclusion morphology, and ultrastructure in HEp-2 cells.

Main Methods:

  • Treatment of HEp-2 cells infected with C. pneumoniae with varying concentrations of IFN-gamma.
  • Assessment of C. pneumoniae replication.
  • Morphological and ultrastructural analysis of bacterial inclusions.

Main Results:

  • IFN-gamma treatment caused a dose-dependent decrease in C. pneumoniae replication.
  • A phenotypic switch was observed, with fewer typical inclusions and more smaller, atypical inclusions.
  • Ultrastructural analysis revealed aberrant bodies within atypical inclusions, lacking redifferentiation into elementary bodies.

Conclusions:

  • IFN-gamma induces an antimicrobial state in HEp-2 cells, inhibiting C. pneumoniae replication.
  • IFN-gamma promotes the formation of atypical C. pneumoniae inclusions with aberrant bodies.
  • These findings offer insights into host-pathogen interactions and potential therapeutic strategies against C. pneumoniae infections.

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