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Effects of piroxicam on mononuclear cells. Comparison with other antiarthritic drugs
Abstract:
Piroxicam and other antiarthritic drugs were compared with respect to their effects on T-lymphocyte/monocyte/rheumatoid synovial cell interactions leading to inflammatory mediator production. Piroxicam inhibited PGE2 formation by blood mononuclear cells, but was less potent than indomethacin. Both drugs enhanced suboptimal phytohemagglutinin (PHA)-stimulated tritiated thymidine (3H-TdR) incorporation by mononuclear cells, although optimal responses were less affected. Exogenous interleukin-2 (IL-2) enhanced suboptimal but not optimal PHA responses, and the effects of the cyclo-oxygenase inhibitors were overcome by exogenous PGE2. Thus piroxicam and indomethacin prevented the inhibition by endogenous monocyte-derived PGE2 of IL-2 secretion and activity. Other antiarthritic drugs, including antimalarials, immunosuppressive agents and gold salts, inhibited PHA-induced lymphocyte proliferation regardless of the level of stimulation. Mepacrine and chloroquine were more effective in inhibiting the release of mononuclear cell factor (MCF) that stimulated PGE2 synthesis by synovial cells. Cyclosporin-A, azathioprine and 6-mercaptopurine were more potent as antiproliferative agents than as inhibitors of mediator release. Sodium aurothiomalate and aurothioglucose selectively interfered with lymphocyte-mediated amplification of MCF release, whereas auranofin inhibited spontaneous production of monocytes and the action of MCF on synovial cells. In rheumatoid synovial cells, piroxicam and indomethacin inhibited PGE2 production but not collagenase release. Suppression of MCF release could lead indirectly to reduction of IL-2 and collagenase as well as PGE2 production and consequently to more profound inhibition of immunologically-mediated inflammation.
Insights
Piroxicam and indomethacin inhibit inflammatory mediator production by affecting T-lymphocyte and monocyte interactions. These drugs, along with others, impact lymphocyte proliferation and cytokine release in inflammatory conditions.
Area of Science:
- Immunology and Pharmacology
- Rheumatology
Background:
- T-lymphocyte, monocyte, and rheumatoid synovial cell interactions drive inflammatory mediator production.
- Non-steroidal anti-inflammatory drugs (NSAIDs) and other antiarthritic agents modulate these interactions.
Purpose of the Study:
- To compare the effects of piroxicam and other antiarthritic drugs on inflammatory mediator production.
- To investigate the impact of these drugs on T-lymphocyte/monocyte/synovial cell interactions.
Main Methods:
- Assessing the inhibition of prostaglandin E2 (PGE2) formation by blood mononuclear cells.
- Evaluating phytohemagglutinin (PHA)-stimulated lymphocyte proliferation and tritiated thymidine incorporation.
- Measuring the effects on interleukin-2 (IL-2) secretion and mononuclear cell factor (MCF) release.
- Examining drug effects on rheumatoid synovial cell collagenase release.
Main Results:
- Piroxicam and indomethacin inhibited PGE2 production by mononuclear cells, with indomethacin being more potent.
- Both drugs enhanced suboptimal PHA-stimulated lymphocyte proliferation, counteracting monocyte-derived PGE2 inhibition of IL-2.
- Other antiarthritic drugs differentially affected lymphocyte proliferation and mediator release; gold salts interfered with MCF amplification, while auranofin affected monocyte production and MCF action.
- Piroxicam and indomethacin inhibited PGE2 but not collagenase release in rheumatoid synovial cells.
Conclusions:
- Piroxicam and indomethacin modulate immune cell interactions and mediator production, potentially reducing inflammation.
- Suppression of MCF release may indirectly decrease IL-2, collagenase, and PGE2, leading to profound anti-inflammatory effects.
- Different classes of antiarthritic drugs exhibit distinct mechanisms of action on immune cells and inflammatory pathways.
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