Description:
<jats:title>ABSTRACT</jats:title>
<jats:p>
<jats:italic>Chlamydia pneumoniae</jats:italic>
may modulate the proliferation of smooth muscle cells (SMC) in atherosclerotic plaques. Conditioned medium from
<jats:italic>C. pneumoniae-</jats:italic>
infected SMC decreased the proliferation of uninfected SMC. Treatment of infected cells with the cyclooxygenase-2 inhibitor NS-398 {
<jats:italic>N</jats:italic>
-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide} suppressed the up-regulation of prostaglandin E
<jats:sub>2</jats:sub>
(PGE
<jats:sub>2</jats:sub>
) and abolished the antimitogenic effect of conditioned medium, suggesting that
<jats:italic>C. pneumoniae</jats:italic>
can decrease SMC proliferation via stimulation of PGE
<jats:sub>2</jats:sub>
synthesis.
</jats:p>