Medizinische Universität Graz - Research portal
Selected Publication:
Tiran, A; Gruber, HJ; Graier, WF; Wagner, AH; Van Leeuwen, EB; Tiran, B.
Aspirin inhibits Chlamydia pneumoniae-induced nuclear factor-kappa B activation, cytokine expression, and bacterial development in human endothelial cells.
Arterioscler Thromb Vasc Biol. 2002; 22(7):1075-1080
Doi: 10.1161/01.ATV.00000022695.22369.BE
[OPEN ACCESS]
Web of Science
PubMed
FullText
FullText_MUG
Google Scholar
- Leading authors Med Uni Graz
- Tiran Andreas
- Co-authors Med Uni Graz
- Graier Wolfgang
- Gruber Hans-Jürgen
- Tiran Beate
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
- OBJECTIVE: Chlamydia pneumoniae has been associated with atherosclerosis. Infection of vascular endothelial cells with C pneumoniae increases the expression of proatherogenic cytokines mediated by nuclear factor (NF)-kappaB, a transcription factor. The present study was designed to test the effect of aspirin on C pneumoniae-induced NF-kappaB activation, interleukin expression, and bacterial development in cultured human endothelial cells. METHODS AND RESULTS: Aspirin, its metabolite salicylic acid, and 2 other unrelated NF-kappaB inhibitors showed a strong concentration-dependent inhibitory effect on chlamydial growth, indicated by the reduction of bacterial inclusions and the titer of infectious progeny. Involvement of the transcription factor NF-kappaB was confirmed by electrophoretic mobility shift assay and by transfection experiments with appropriate decoy oligodeoxynucleotides. Attenuation of the C pneumoniae-induced activation of NF-kappaB by aspirin also reduced the secretion of interleukin-6 and interleukin-8, indicating efficient inhibition of NF-kappaB gene expression. Reduction of chlamydial growth was not caused by apoptosis of the host cell, as determined by monitoring characteristic chromatin condensation. CONCLUSIONS: These data provide evidence that NF-kappaB-mediated gene activation represents a crucial step in the developmental cycle of C pneumoniae. Aspirin exerts an anti-chlamydial effect that is due to the inhibition of C pneumoniae-induced NF-kappaB activation, which might account for some of the cardioprotective activity of aspirin.
- Find related publications in this database (using NLM MeSH Indexing)
- Apoptosis - drug effects
- Aspirin - pharmacology
- Cell Line - pharmacology
- Chlamydophila pneumoniae - drug effects
- Endothelium, Vascular - drug effects
- Humans - drug effects
- Interleukin-6 - antagonists and inhibitors
- Interleukin-8 - antagonists and inhibitors
- NF-kappa B - antagonists and inhibitors
- Umbilical Veins - antagonists and inhibitors
- Find related publications in this database (Keywords)
- aspirin
- transcription factor
- Chlamydia pneumoniae
- nuclear factor-K beta