Effects of COX-2 inhibitors on ROS produced by Chlamydia pneumoniae

Biochem Biophys Res Commun. 2004 Dec 24;325(4):1122-30.Click here to read Links
    Effects of COX-2 inhibitors on ROS produced by Chlamydia pneumoniae-primed human promonocytic cells (THP-1).
    Mouithys-Mickalad A, Deby-Dupont G, Dogne JM, de Leval X, Kohnen S, Navet R, Sluse F, Hoebeke M, Pirotte B, Lamy M.

    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

    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.

This may be why ibruprophen seems to work well for me in combating Cpn induced inflammation. There is also discussion in some related articles on Cpn reduction of inflammation being the origin of the effects of aspirin in reducing heart disease, i.e. that it acts on Cpn induced inflammation. COX-Inhibitors in general also seem to but a halt to further Cpn growth, although do not reduce infection currently in place.

I'll be interested in Red's take on all this, as the COX-2's have other effects he has noted which are perhaps less good for bacterial problems.


CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral


 Hi Jim,

Interesting.   I do use Ibuprofen, but I use it only sparingly for reasons I've mentioned here:


That said, I have found that Ibuprofen seems to work very well to shut down negative reactions I may be having.    I've come to suspect myself that Ibuprofen may work its magic for me by some effect it has related to reactive oxygen species.   With a little googling, I found this:

Arachidonate and NADPH oxidase synergise with iNOS to induce death in macrophages: mechanisms of inflammatory degeneration.

Ibuprofen seems to shut down reactions that I suspect are related to elevated secondary porphyria levels for me, and it works very quickly.  I'm wondering if it is preventing / blocking reaction to ROS (generated by the secondary porphyria)?    I'm not sure.   I'm just wondering...



Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-