The main aim of this study has been to determine the effect of selected non-steroidal anti-inflammatory drugs (NSAIDs) – depending on their selectivity to cyclooxygenase (COX) 1 and 2 –… Click to show full abstract
The main aim of this study has been to determine the effect of selected non-steroidal anti-inflammatory drugs (NSAIDs) – depending on their selectivity to cyclooxygenase (COX) 1 and 2 – on the activation-induced CD25 expression on CD4+ and CD8+ T cells. Lymphocytes obtained from lymph nodes of mice were treated with acetylsalicylic acid (ASA; a preferential COX-1 inhibitor), ketoprofen (KET; a non-selective COX inhibitor) and robenacoxib (ROB; a selective COX-2 inhibitor) in concentrations reflecting their plasma levels achieved in vivo at therapeutic doses and in ten-fold lower concentrations. The cells were activated with concanavalin A. In contrast to KET and ROB, ASA had no effect on the activation-induced CD25 expression on CD4+ and CD8+ T cells, nor did it affect the counts of CD4+ and CD8+ activated effector (aTeff) and resting (Trest) T cells. Both KET and ROB caused a depletion of CD8+ aTeff cells, and additionally KET induced a loss of CD8+ Trest cells. Moreover, ROB, but not the other drugs, reduced the activation-induced CD25 expression on CD4+ T cells. This suggests that non-selective COX inhibitors and selective COX-2 inhibitors may weaken the effector T cell response by producing a negative effect on the count of aTeff cells. Furthermore, the results seem to imply that ASA and KET have certain potential to induce Foxp3 expression in CD25+CD8+ and CD25+CD4+ T cells, respectively. However, all the observed changes were very weakly manifested and therefore it is not certain whether they have clinical importance, despite the statistical significance determined.
               
Click one of the above tabs to view related content.