TY - JOUR
T1 - Cortisol is not the primary mediator for augmented CXCR4 expression on natural killer cells after acute exercise
AU - Okutsu, Mitsuharu
AU - Ishii, Kenji
AU - Niu, Kaijun
AU - Nagatomi, Ryoichi
PY - 2014/8/1
Y1 - 2014/8/1
N2 - CXC-chemokine receptor 4 (CXCR4) and its ligand, stromal-derived factor 1α (SDF-1α; also known as CXCL12), are crucial for the redistribution of immune cells after acute exercise. We investigated the relationships between acute exercise and CXCR4 expression on natural killer (NK) cells. Peripheral blood mononuclear cells (PBMCs) were cultured with cortisol and analyzed for CXCR4 expression on CD3-/CD56+ NK cells and NK cell migration activity. To determine the effect of exercise, we isolated PBMCs from subjects before and after a 90-min exercise at 70% peak O 2 uptake (VO2peak) and determined the changes in CXCR4 expression on NK cells after exercise. We cultured PBMCs with plasma obtained before and after exercise and with the glucocorticoid antagonist RU-486 to determine NK cell migration activity and the effects of cortisol on CXCR4 expression in vitro. Cortisol treatment increased CXCR4 expression (P < 0.05) and migration activity (P < 0.05) of NK cells. Exercise did not affect CXCR4 expression on NK cells, whereas incubating them with postexercise plasma significantly increased CXCR4 expression (P < 0.05) and migration activity (P < 0.05). RU-486 blocked cortisol-induced CXCR4 upregulation on NK cells, but only partially blocked (7%) CXCR4 upregulation when PMBCs were incubated with postexercise plasma. Thus acute exercise increases CXCR4 expression on NK cells and their migration activity and may contribute to NK cell redistribution after acute exercise; however, cortisol did not appear to be the primary mediator of augmented CXCR4 expression.
AB - CXC-chemokine receptor 4 (CXCR4) and its ligand, stromal-derived factor 1α (SDF-1α; also known as CXCL12), are crucial for the redistribution of immune cells after acute exercise. We investigated the relationships between acute exercise and CXCR4 expression on natural killer (NK) cells. Peripheral blood mononuclear cells (PBMCs) were cultured with cortisol and analyzed for CXCR4 expression on CD3-/CD56+ NK cells and NK cell migration activity. To determine the effect of exercise, we isolated PBMCs from subjects before and after a 90-min exercise at 70% peak O 2 uptake (VO2peak) and determined the changes in CXCR4 expression on NK cells after exercise. We cultured PBMCs with plasma obtained before and after exercise and with the glucocorticoid antagonist RU-486 to determine NK cell migration activity and the effects of cortisol on CXCR4 expression in vitro. Cortisol treatment increased CXCR4 expression (P < 0.05) and migration activity (P < 0.05) of NK cells. Exercise did not affect CXCR4 expression on NK cells, whereas incubating them with postexercise plasma significantly increased CXCR4 expression (P < 0.05) and migration activity (P < 0.05). RU-486 blocked cortisol-induced CXCR4 upregulation on NK cells, but only partially blocked (7%) CXCR4 upregulation when PMBCs were incubated with postexercise plasma. Thus acute exercise increases CXCR4 expression on NK cells and their migration activity and may contribute to NK cell redistribution after acute exercise; however, cortisol did not appear to be the primary mediator of augmented CXCR4 expression.
KW - Cell distribution
KW - Chemokine receptor
KW - Cortisol
KW - Exercise
KW - Natural killer cells
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U2 - 10.1152/japplphysiol.00176.2014
DO - 10.1152/japplphysiol.00176.2014
M3 - Article
C2 - 24947029
AN - SCOPUS:84905503641
VL - 117
SP - 199
EP - 204
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 3
ER -