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Aspirin inhibits Chlamydia pneumoniae-induced nuclear factor-kappa B activation, cytokine expression, and bacterial

Andreas Tiran1, Hans-Jürgen Gruber, Wolfgang F Graier

  • 1Department of Laboratory Medicine, University of Graz, Austria. andreas.tiran@uni-graz.at

Arteriosclerosis, Thrombosis, and Vascular Biology
|July 16, 2002
PubMed

Insights

Aspirin inhibits Chlamydia pneumoniae growth by blocking nuclear factor-kappaB (NF-kappaB) activation. This anti-chlamydial effect may contribute to aspirin's cardioprotective benefits.

Area of Science:

  • Microbiology
  • Cardiovascular Science
  • Molecular Biology

Background:

  • Chlamydia pneumoniae infection is linked to atherosclerosis.
  • C. pneumoniae infection elevates proatherogenic cytokines via nuclear factor-kappaB (NF-kappaB) activation in endothelial cells.

Purpose of the Study:

  • To investigate aspirin's impact on C. pneumoniae-induced NF-kappaB activation.
  • To assess aspirin's effect on interleukin expression and bacterial development in human endothelial cells.

Main Methods:

  • Assessed aspirin's effect on C. pneumoniae growth, NF-kappaB activation, and interleukin secretion.
  • Utilized electrophoretic mobility shift assay and transfection experiments to confirm NF-kappaB involvement.
  • Monitored host cell apoptosis to rule out this mechanism for growth reduction.

Main Results:

  • Aspirin, salicylic acid, and NF-kappaB inhibitors demonstrated concentration-dependent inhibition of C. pneumoniae growth.
  • Aspirin attenuated C. pneumoniae-induced NF-kappaB activation, reducing interleukin-6 and interleukin-8 secretion.
  • Chlamydial growth reduction was not due to host cell apoptosis.

Conclusions:

  • NF-kappaB-mediated gene activation is vital for C. pneumoniae development.
  • Aspirin's anti-chlamydial activity, via NF-kappaB inhibition, may explain its cardioprotective effects.
Abstract

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