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Strenuous Exercise Enhances Platelet‐Impeded Apoptosis of Nasopharyngeal Carcinoma by Natural Killer Cell in Men
Author(s) -
Chung Yi,
Wang JongShyan
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a812-d
Subject(s) - granzyme b , apoptosis , perforin , platelet , nasopharyngeal carcinoma , natural killer cell , immunology , medicine , chemistry , immune system , cytotoxicity , cd8 , biochemistry , radiation therapy , in vitro
Natural killer cells (NKCs) can induce the death of carcinoma cell by engaging the perforin/granzyme‐mediated cytotoxicity, whereas platelets attenuate the ability of NKCs destroying carcinoma cell. Exercise is associated with intensity‐dependent immune response and platelet reactivity. This study was to investigate how short‐term exercise affects platelet‐mediated apoptosis of nasopharyngeal carcinoma cell (NPC) by NKC and its underlying mechanisms. Moderate exercise (60% VO 2 max for 40 min; ME) and strenuous exercise (up to VO 2 max; SE) on a bicycle ergometer in 17 sedentary healthy men were executed on two separate occasions. Blood samples were collected before and immediately after exercise. Leukocyte and platelets counts, intracellular perforin and granzyme B contents in NK cells, and apoptosis of NPC by NKC were determined. Analytical results demonstrated that (1) SE increased NKC and platelet concentration in blood, and was accompanied by an elevation in perforin and granzym B levels of NKC; (2) Apoptosis of NPC by NKC was enhanced by SE, whereas co‐incubating NKC with platelet attenuated the NKC‐NPC interaction and the ability of tumor apoptosis induced by NKC following this exercise; and (3) Although ME increased NKC interaction with NPC and subsequently enhanced apoptosis of NPC by NKC, there were not significant changes in platelet counts and intracellular perforin and granzyme B contents in NKCs, as well as platelet‐mediated apoptosis of NPC by NKC following this exercise. We conclude that both SE and ME can enhance apoptosis of NPC by NKC. However, platelet functional changes induced by SE, but not ME, attenuate the tumor apoptosis induced by NKC.