The effect of sulphasalazine on the in vitro activation of human peripheral blood mononuclear cells by phytohemagglutinin P.
Sérgio Pacheco, Jones Db, Keith Hillier
Abstract
Sérgio Pacheco, Jones Db, Keith Hillier
Abstract
The in vitro action of sulphasalazine, BW 755-C and indomethacin on phytohemagglutinin P-induced human peripheral blood mononuclear cell activation was studied. Sulphasalazine increased, while indomethacin and BW 755-C decreased, prostaglandin E2 (PGE2) accumulation in activated cultures. When used together with indomethacin or BW 755-C, sulphasalazine did not counteract the inhibition of PGE2 caused by the other two. Sulphasalazine inhibited phytohemagglutinin P-induced cell activation in a concentration-dependent manner even when used together with indomethacin or BW 755-C. BW 755-C inhibited cell activation at 350 microM, whereas at 11 microM it only increased sulphasalazine-induced inhibition. The implications of these findings on the etiopathology of inflammatory bowel disease are discussed.
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The in vitro action of sulphasalazine, BW 755-C and indomethacin on phytohemagglutinin P-induced human peripheral blood mononuclear cell activation was studied. Sulphasalazine increased, while indomethacin and BW 755-C decreased, prostaglandin E2 (PGE2) accumulation in activated cultures. When used together with indomethacin or BW 755-C, sulphasalazine did not counteract the inhibition of PGE2 caused by the other two. Sulphasalazine inhibited phytohemagglutinin P-induced cell activation in a concentration-dependent manner even when used together with indomethacin or BW 755-C. BW 755-C inhibited cell activation at 350 microM, whereas at 11 microM it only increased sulphasalazine-induced inhibition. The implications of these findings on the etiopathology of inflammatory bowel disease are discussed.
Key concepts: Peripheral blood mononuclear cell, In vitro, Prostaglandin E2, Chemistry, Prostaglandin E, Peripheral blood, Prostaglandin, Peripheral