Blockade of P-Selectin Reduces Neutrophil Infiltration Into the Ischemia-Reperfusion Induced Murine Testis

Abstract

Germ cell apoptosis after ischemia-reperfusion (IR) of the testis 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 to the IR- induced testis 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 the function-blocking monoclonal P-selectin antibody (FBMAB group) or the isotype-matched control antibody (IMCA group). Separate groups of mice underwent a sham operation (SO group) or received 500 ng of TNF alpha (IF group) to induce inflammation. Mice were sacrificed 24 hr 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 to the IR-induced testis significantly. Therefore, blocking P-selectin may be therapeutically beneficial to protect postischemic testis.