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Aspirin inhibits Chlamydia pneumoniae-induced NF-kappaB activation, cyclo-oxygenase-2 expression and prostaglandin E2 synthesis and attenuates chlamydial growth
2003
Journal of Medical Microbiology
Infection with Chlamydia pneumoniae has been implicated as a potential risk factor for atherosclerosis. This study was designed to investigate the mechanisms of the anti-chlamydial activity of aspirin. A reporter gene assay for NF-kB activity, immunoblot analysis for cyclo-oxygenase (COX)-2 and radioimmunoassay for prostaglandin E 2 (PGE 2 ) were performed. Following infection of HEp-2 cells with C. pneumoniae, NF-kB was activated, COX-2 was induced and PGE 2 was elevated. Aspirin inhibited
doi:10.1099/jmm.0.04992-0
pmid:12721317
fatcat:pe6st4ut5vhonchaesmm3xkqwm