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Chlamydia pneumoniae decreases smooth muscle cell proliferation through induction of prostaglandin E2 synthesis

Jürgen Rödel1, Dirk Prochnau, Katrin Prager

  • 1Institute of Medical Microbiology, Friedrich Schiller University of Jena, Semmelweisstr. 4, D-07740 Jena, Germany. juergen.roedel@med.uni-jena.de

Infection and Immunity
|July 24, 2004
PubMed

Insights

Chlamydia pneumoniae infection in smooth muscle cells reduces their proliferation. This effect is mediated by prostaglandin E(2), suggesting a new therapeutic target for atherosclerosis.

Area of Science:

  • Cardiovascular Research
  • Infectious Diseases
  • Cell Biology

Background:

  • Atherosclerosis involves smooth muscle cell (SMC) proliferation within plaques.
  • Chlamydia pneumoniae is a potential contributor to cardiovascular disease pathogenesis.

Purpose of the Study:

  • To investigate the effect of Chlamydia pneumoniae on SMC proliferation.
  • To elucidate the mechanism by which C. pneumoniae influences SMC proliferation.

Main Methods:

  • SMC were infected with C. pneumoniae.
  • Conditioned medium from infected SMC was used to treat uninfected SMC.
  • The cyclooxygenase-2 inhibitor NS-398 was used to block prostaglandin E(2) synthesis.

Main Results:

  • Conditioned medium from C. pneumoniae-infected SMC inhibited the proliferation of uninfected SMC.
  • NS-398 treatment suppressed prostaglandin E(2) up-regulation in infected cells.
  • Inhibition of prostaglandin E(2) abolished the anti-proliferative effect of the conditioned medium.

Conclusions:

  • Chlamydia pneumoniae decreases SMC proliferation.
  • Prostaglandin E(2) synthesis is a key mediator of this anti-proliferative effect.
  • Targeting prostaglandin E(2) may offer a therapeutic strategy for C. pneumoniae-related atherosclerosis.

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