Exercise affects platelet-impeded antitumor cytotoxicity of natural killer cell

Natural killer cells (NK) induce the death of tumor cells by perforin/granzyme-mediated cytotoxicity, whereas platelets reduce the capacity of NK to destroy tumor cells. Physical exercise affects both immune function and platelet activity because responses depend on type, intensity, and duration of exercise. This investigation explores how various exercise regimens influence platelet-impeded cytotoxicity of NK to nasopharyngeal carcinoma cells (NPC).

Thirty sedentary men performed on three occasions moderate exercise (60% .VO2max for 40 min), severe exercise (up to .VO2max), and severe exercise after warm-up exercise (60% .VO2max for 20 min). NK count and perforin/granzyme B contents, NK-NPC binding, and NK-induced NPC apoptosis were measured using a flow cytometer, whereas NK-induced NPC detachment from collagen-coated surface was determined using an electrical cell-substrate impedance sensing.

Severe exercise enhanced NK-induced NPC caspase-3 activation, phosphatidylserine (PS) exposure, DNA fragmentation, and detachment and was accompanied by increased NK count and perforin/granzyme B contents (P < 0.05). Moreover, severe exercise simultaneously promoted the suppression of platelet to NK-NPC binding and NK-induced NPC caspase-3 and -8 activations, PS exposure, DNA fragmentation, and detachment (P < 0.05). However, warm-up exercise pretreatment diminished the effects of severe exercise in platelet-impeded NK-NPC binding and NK-induced NPC apoptosis. Although moderate exercise also suppressed platelet-impeded NK-NPC interaction (P < 0.05), no significant changes occurred in NK count and perforin/granzyme B contents after this exercise.

Severe exercise enhances the cytotoxicity of NK to NPC and simultaneously promotes the platelet-impeded apoptosis of NPC induced by NK. However, warm-up exercise reduces the resistance of platelet to NK-NPC interaction, increasing the efficiency of anti-NPC cytotoxicity by NK after severe exercise.