Effects of COX-2 inhibitors on ROS produced by Chlamydia pneumoniae-primed human promonocytic cells (THP-1)

Ange Mouithys-Mickalad, Ginette Deby-Dupont, Jean-Michel Dogne, Xavier de Leval, Stephan Kohnen, Rachel Navet, Francis Sluse, Maryse Hoebeke, Bernard Pirotte, Maurice Lamy

Research output: Contribution to journalArticlepeer-review


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.
Original languageEnglish
Pages (from-to)1122-30
Number of pages9
JournalBiochemical and Biophysical Research Communications
Issue number4
Publication statusPublished - 24 Dec 2004


  • Arteriosclerosis
  • Cell Differentiation
  • Cell Line
  • Chlamydophila pneumoniae
  • Cyclooxygenase Inhibitors
  • Dose-Response Relationship, Drug
  • Free Radicals
  • Humans
  • Inflammation
  • Macrophages
  • Monocytes
  • Reactive Oxygen Species
  • Tetradecanoylphorbol Acetate


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