BACKGROUND: Cyclooxygenase-2 (COX-2) is up-regulated by a variety of stimuli that are associated with tissue injury and inflammation. METHODS: The purpose of this study was to analyze COX-2 detection during different grades of acute human renal allograft rejection. COX-2 expressions were analyzed by immunohistochemistry in 74 samples obtained from biopsies with acute rejection of different grades (n= 48), tubular changes (n=13) and from kidney allografts with stable function (n=13). RESULTS: In interstitial area, there was a significant correlation of COX-2 induction in acute rejection in comparison to tubular changes (1.67 vs. 0.76, p=0.02) and stable function (vs. 0.07, p<0.001), as well as in vessels in the group with acute rejection in relation to stable function (1.1 vs. 0, p=0.04). When the group with acute rejection was analyzed in subgroups, there was a clear increase of COX-2 expression from acute rejection grade IB to III in vessels, in inflammatory infiltrating cells in interstitial area and in glomeruli, while borderline and IA grades were intermediate. CONCLUSION: COX-2 is up-regulated during acute human renal allograft rejection according to the severity of acute rejection and could be used as a marker of inflammation in kidney transplantation.
BACKGROUND:Cyclooxygenase-2 (COX-2) is up-regulated by a variety of stimuli that are associated with tissue injury and inflammation. METHODS: The purpose of this study was to analyze COX-2 detection during different grades of acute human renal allograft rejection. COX-2 expressions were analyzed by immunohistochemistry in 74 samples obtained from biopsies with acute rejection of different grades (n= 48), tubular changes (n=13) and from kidney allografts with stable function (n=13). RESULTS: In interstitial area, there was a significant correlation of COX-2 induction in acute rejection in comparison to tubular changes (1.67 vs. 0.76, p=0.02) and stable function (vs. 0.07, p<0.001), as well as in vessels in the group with acute rejection in relation to stable function (1.1 vs. 0, p=0.04). When the group with acute rejection was analyzed in subgroups, there was a clear increase of COX-2 expression from acute rejection grade IB to III in vessels, in inflammatory infiltrating cells in interstitial area and in glomeruli, while borderline and IA grades were intermediate. CONCLUSION:COX-2 is up-regulated during acute human renal allograft rejection according to the severity of acute rejection and could be used as a marker of inflammation in kidney transplantation.
Authors: Jonathan Kunisch Eriksen; Lise H Nielsen; Niels Moeslund; Anna K Keller; Søren Krag; Michael Pedersen; Jens Aage K Pedersen; Henrik Birn; Bente Jespersen; Rikke Norregaard Journal: Anesth Analg Date: 2020-03 Impact factor: 5.108