title: Effects of COX-2 inhibitors on ROS produced by Chlamydia pneumoniae-primed human promonocytic cells (THP-1).
abstract: Chronic inflammation through foam cells and macrophages is important in atherosclerosis development, and can be considered as therapeutic targets. Cyclooxygenase and NADPH-oxidase were expressed within atherosclerotic lesions. Reactive oxygen species produced by NADPH oxidase were found to trigger the cyclooxygenase-2 expression. The effects of preferential COX-2 inhibitors on ROS produced by Chlamydia-primed human monocytes (THP-1 cells) were evaluated by fluorescence, chemiluminescence, oxymetry, and EPR spin trapping. Fluorescence assays showed an increased production of ROS with Chlamydia versus cells primed by 10(-8)M PMA. COX-2 inhibitors inhibited in a dose-dependent manner the luminol-enhanced CL while ibuprofen and diclofenac increased the chemiluminescence response. By EPR spin trapping, COX-2 inhibitors, ibuprofen, and diclofenac, exhibited a dose-dependent inhibiting effect (10 and 100muM) on the EPR signal appearance. Our cell model combining EPR, chemiluminescence, and oxymetry appeared relevant to study the modulating effects of preferential COX-2 inhibitors on the cell oxidant activity and chronic inflammatory diseases.
authors.affiliation: Centre for Oxygen, Research and Development (C.O.R.D.), Institut de Chimie, B6a, University of Liège, Sart Tilman, 4000 Liège, Belgium. amouithys@ulg.ac.be
authors.forename: Ange
authors.initials: A
authors.lastname: Mouithys-Mickalad
authors.forename: Ginette
authors.initials: G
authors.lastname: Deby-Dupont
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Dogne
authors.forename: Xavier
authors.initials: X
authors.lastname: de Leval
authors.forename: Stephan
authors.initials: S
authors.lastname: Kohnen
authors.forename: Rachel
authors.initials: R
authors.lastname: Navet
authors.forename: Francis
authors.initials: F
authors.lastname: Sluse
authors.forename: Maryse
authors.initials: M
authors.lastname: Hoebeke
authors.forename: Bernard
authors.initials: B
authors.lastname: Pirotte
authors.forename: Maurice
authors.initials: M
authors.lastname: Lamy
mesh_terms: D001161:Arteriosclerosis / Q000378:metabolism / Q000517:prevention & control; D002454:Cell Differentiation; D002460:Cell Line; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D008264:Macrophages / Q000166:cytology / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology; D009000:Monocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism* / Q000382:microbiology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D016861:Cyclooxygenase Inhibitors; D005609:Free Radicals; D017382:Reactive Oxygen Species; D013755:Tetradecanoylphorbol Acetate