01930nas a2200229   4500000000100000000000100001008004100002260004400043653001500087653001600102653001300118653001100131653001200142100001300154700000500167700001100172245011600183300001200299490000800311520136700319022001401686       2008                            d  c12/2008bM. & H. Schaper GmbHaHannover10aantibodies10aneutrophils10aselectin10atestis10atorsion1 aM Celebi1 a1 aA Paul00aBlockade of p-selectin reduces neutrophil infiltration into the murine testis after ischemia-reperfusion-injury  a457-4600 v1153 aGerm cell specific apoptosis after ischemia-reperfusion (I/R) induced testicular injury is dependent on neutrophil recruitment to the testis. Intravascular adhesion molecules like the P- and E- selectins play an important role in this recruitment. The purpose of this study was to inhibit neutrophil recruitment in I/R induced testicular injury by using a function-blocking monoclonal anti-mouse P-selectin antibody. Adult mice were subjected to a 2 h period of testicular torsion (ischemia) followed by detorsion (reperfusion). Ten minutes after the onset of reperfusion, mice received either 100  amp;#956;g of a function-blocking monoclonal P-selectin antibody (FBMAB group) or isotype-matched control antibody (IMCA group). Separate groups of mice underwent sham-operation (SO group) or received 500 ng of TNFM (IF group) to induce inflammation. Mice were sacrificed 24 h after reperfusion and testiscular interstitial cells were isolated and analyzed for the presence of neutrophils by means of flow cytometry. The function-blocking monoclonal P-selectin antibody reduced neutrophil recruitment in I/R induced testicular injury significantly (FBMAB group as compared to the IMCA group 26 ± 4 vs. 52 ± 10% Gr #150;1+CD11b+ of total leucocytes; P  lt; 0.001). Therefore, blocking P-selectin may be therapeutically beneficial to protect postischemic testis.   a0341-6593