Chlamydia pneumoniae decreases smooth muscle cell proliferation through induction of prostaglandin E2 synthesis.
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.
Institute of Medical Microbiology, Friedrich Schiller University of Jena, Semmelweisstr. 4, D-07740 Jena, Germany. juergen.roedel@med.uni-jena.de
Jürgen
J
Rödel
Dirk
D
Prochnau
Katrin
K
Prager
Jürgen
J
Baumert
Karl-Hermann
KH
Schmidt
Eberhard
E
Straube
D002455:Cell Division; D002478:Cells, Cultured; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity*; D017077:Culture Media, Conditioned; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000096:biosynthesis*; D006801:Humans; D032389:Myocytes, Smooth Muscle / Q000166:cytology* / Q000382:microbiology*; D009578:Nitrobenzenes / Q000494:pharmacology; D013449:Sulfonamides / Q000494:pharmacology; D015854:Up-Regulation
D017077:Culture Media, Conditioned; D016861:Cyclooxygenase Inhibitors; D009578:Nitrobenzenes; D013449:Sulfonamides; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D015232:Dinoprostone