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Chlamydia pneumoniae decreases smooth muscle cell proliferation through induction of prostaglandin E2 synthesis
Authors:Rödel Jürgen  Prochnau Dirk  Prager Katrin  Baumert Jürgen  Schmidt Karl-Hermann  Straube Eberhard
Affiliation:Institute of Medical Microbiology, Friedrich Schiller University of Jena, Semmelweisstr. 4, D-07740 Jena, Germany. juergen.roedel@med.uni-jena.de
Abstract:Chlamydia pneumoniae may modulate the proliferation of smooth muscle cells (SMC) in atherosclerotic plaques. Conditioned medium from C. pneumoniae-infected SMC decreased the proliferation of uninfected SMC. Treatment of infected cells with the cyclooxygenase-2 inhibitor NS-398 [N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide] suppressed the up-regulation of prostaglandin E(2) (PGE(2)) and abolished the antimitogenic effect of conditioned medium, suggesting that C. pneumoniae can decrease SMC proliferation via stimulation of PGE(2) synthesis.
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