Infection and Immunity · 2004 · 10 citations · 20 references
Life SciencesCell BiologyPharmacologyCell SignalingInflammationMetabolismAtherosclerosis PharmacotherapyEicosanoid BiosynthesisCyclooxygenase InhibitorsCyclooxygenase Pathway SignalingCyclooxygenase-2 PathwayProstaglandin ActivityProstaglandin ModulationProstaglandin ProductionProstaglandin SignalingProstaglandin Synthesis Inhibition
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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Francesco Cipollone, Cesaria Prontera, Barbara Pini et al. · Circulation · 2001 · 349 citations · Full text
Sebastian Sasu, David LaVerda, Nilofer Qureshi et al. · Circulation Research · 2001 · 279 citations · Full text