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The acute phase reactant response to respiratory infection with Chlamydia pneumoniae: implications for the

Lee Ann Campbell1, Kambiz Yaraei, Brian Van Lenten

  • 1Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA 98195, USA.

Microbes and Infection
|April 27, 2010
PubMed

Insights

Chlamydia pneumoniae infection triggers an acute phase response in mice, increasing inflammatory proteins and decreasing HDL

Area of Science:

  • Infectious Diseases
  • Immunology
  • Cardiovascular Research

Background:

  • Chlamydia pneumoniae is a pathogen linked to cardiovascular disease.
  • The acute phase response involves systemic changes in host physiology during infection.
  • Atherosclerotic plaque stability is crucial in cardiovascular event pathogenesis.

Purpose of the Study:

  • To investigate the acute phase response to Chlamydia pneumoniae infection in mice.
  • To assess the impact of this response on atherosclerotic plaque stability.

Main Methods:

  • Mice were infected intranasally with Chlamydia pneumoniae.
  • Plasma cytokine and acute phase protein levels were measured.
  • Paraoxonase activity and HDL's oxidative protection were assessed.
  • Intra-plaque hemorrhage frequency was analyzed in apolipoprotein E-deficient mice.

Main Results:

  • Infection increased plasma levels of IL-2, IL-5, IL-6, IL-10, IL-12, GM-CSF, IFN-gamma, and serum amyloid A.
  • Paraoxonase activity and HDL's protective function decreased post-infection.
  • Older infected mice showed increased intra-plaque hemorrhage compared to controls.

Conclusions:

  • Chlamydia pneumoniae infection elicits a significant acute phase response.
  • This response, characterized by specific inflammatory markers and reduced HDL function, may promote atherosclerotic lesion destabilization.
  • Acute phase proteins contribute to plaque progression and hemorrhage risk.

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