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Effect of nitric oxide on the growth of Chlamydophila pneumoniae

Caterina Romano Carratelli1, Antonietta Rizzo, Rossella Paolillo

  • 1Dept. of Experimental Medicine, Section of Microbiology and Clinical Microbiology, 2nd University of Naples, Via S.M. Di Costantinopoli, 16-80138 Naples, Italy. caterina.romano@unina2.it

Canadian Journal of Microbiology
|December 8, 2005
PubMed

Insights

Nitric oxide (NO) released by immune cells can inhibit Chlamydophila pneumoniae growth and damage the bacteria. This suggests NO plays a role in controlling Chlamydia infections and preventing their spread.

Area of Science:

  • Immunology
  • Microbiology
  • Pathogenesis

Background:

  • Chlamydophila pneumoniae is a significant human pathogen.
  • The pathogenesis and immune control mechanisms of C. pneumoniae infections are not fully understood.
  • The role of nitric oxide (NO) in host defense against C. pneumoniae is unclear.

Purpose of the Study:

  • To investigate the role of the nitric oxide synthase pathway in inhibiting C. pneumoniae infection in macrophage cells.
  • To determine the effect of NO on the viability of isolated C. pneumoniae.

Main Methods:

  • Murine macrophage J774 cells were infected with C. pneumoniae.
  • Recombinant murine gamma interferon (MurIFN-gamma) was used to stimulate NO production.
  • A NO-releasing agent (2-(N,N-diethylamino)-diazenolase-2-oxide) was added before infection or during cultivation.
  • Bacterial viability was assessed.

Main Results:

  • MurIFN-gamma exposure increased NO production and reduced C. pneumoniae viability.
  • Addition of the NO-releasing agent reduced C. pneumoniae viability in a dose-dependent manner.
  • NO demonstrated direct damage to isolated C. pneumoniae.

Conclusions:

  • Immune control of C. pneumoniae in murine macrophages involves NO release.
  • NO exhibits antimicrobial activity against C. pneumoniae.
  • NO may be a key factor in preventing the systemic spread of Chlamydia infections.

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