| Literature DB >> 15271958 |
Jürgen Rödel1, Dirk Prochnau, Katrin Prager, Jürgen Baumert, Karl-Hermann Schmidt, Eberhard Straube.
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.Entities:
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Year: 2004 PMID: 15271958 PMCID: PMC470606 DOI: 10.1128/IAI.72.8.4900-4904.2004
Source DB: PubMed Journal: Infect Immun ISSN: 0019-9567 Impact factor: 3.441