title: Cortisol is not the primary mediator for augmented CXCR4 expression on natural killer cells after acute exercise.
abstract: 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 O2 uptake (V̇o2peak) 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.
authors.affiliation: Faculty of Sport Sciences, Waseda University, Tokorozawa, Saitama, Japan; Institute for Biomedical Engineering, Consolidated Research Institute for Advanced Science and Medical Care, Waseda University, Tokyo, Japan; Graduate School of Natural Sciences, Nagoya City University, Nagoya, Japan okutsu@nsc.nagoya-cu.ac.jp.
authors.forename: Mitsuharu
authors.initials: M
authors.lastname: Okutsu
authors.affiliation: Nanodevice Engineering, Graduate School of Biomedical Engineering, Tohoku University, Sendai, Japan;
authors.forename: Kenji
authors.initials: K
authors.lastname: Ishii
authors.affiliation: Department of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin, China;
authors.forename: Kaijun
authors.initials: K
authors.lastname: Niu
authors.affiliation: Department of Medicine and Science in Sports and Exercise, Tohoku University Graduate School of Medicine, Sendai, Japan; and.
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Nagatomi
mesh_terms: D000328:Adult; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D006801:Humans; D006854:Hydrocortisone / Q000037:antagonists & inhibitors / Q000378:metabolism*; D007694:Killer Cells, Natural / Q000187:drug effects / Q000378:metabolism*; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D015735:Mifepristone / Q000494:pharmacology; D010100:Oxygen / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000378:metabolism*; D055815:Young Adult
chemical_list: C527276:CXCR4 protein, human; D019718:Receptors, CXCR4; D015735:Mifepristone; D010100:Oxygen; D006854:Hydrocortisone
keywords: cell distribution; chemokine receptor; cortisol; exercise; natural killer cells