Blockade of p-selectin reduces neutrophil infiltration into the murine testis after ischemia-reperfusion-injury

Abstract

Germ 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 mu 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 TNF alpha (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 A induced testicular injury significantly (FBMAB group as compared to the IMCA group 26 +/- 4 vs. 52 +/- 10% Gr-1 + CD11b+ of total leucocytes; P < 0.001),Therefore, blocking P-selectin may be therapeutically beneficial to protect postischemic testis.