title: The effects of acute exercise-induced cortisol on CCR2 expression on human monocytes.
abstract: CC-chemokine receptor 2 (CCR2) and its ligand, monocyte chemotactic protein-1 (MCP-1, also known as CCL2), are crucial for the recruitment of monocytes/macrophages to sites of inflammation. We conducted a series of experiments to investigate the relationship between stress, monocyte CCR2 expression and migration activity. First, we collected peripheral blood mononuclear cells (PBMC) from untrained subjects (n=8) and measured CCR2 expression on CD14(+) monocytes cultured with cortisol, epinephrine and norepinephrine. Second, we collected PBMC from the subjects before and after they cycled for 60 min at 70% peak O(2) uptake (VO2(peak)), and measured alterations in CCR2 expression on monocytes following exercise. Third, we cultured PBMC with serum obtained before and after exercise and the glucocorticoid antagonist RU-486 to determine the effect of cortisol on CCR2 expression in vitro. Last, we measured the ability of PBMC treated with serum or cortisol to migrate through membrane filters in response to CCL2. Cortisol (but not epinephrine or norepinephrine) increased CCR2 expression on monocytes in a dose- and time-dependent manner. Exercise did not influence CCR2 expression on PBMC, whereas incubation of PBMC with post-exercise serum significantly increased CCR2 expression. Both cortisol and post-exercise serum increased the migration of PBMC toward CCL2. The increase in CCR2 expression on PBMC following stimulation with cortisol and serum was blocked by the glucocorticoid receptor antagonist RU-486. In conclusion, cortisol released during exercise increased monocyte CCR2 expression and migration activity in vitro. These alterations may influence inflammation and regeneration of damaged tissue after acute stress.
authors.affiliation: Institute for Biomedical Engineering, Consolidated Research Institute for Advanced Science and Medical Care, Waseda University, Tokyo, Japan. Electronic address: okutsu@waseda.jp.
authors.forename: Mitsuharu
authors.initials: M
authors.lastname: Okutsu
authors.affiliation: Faculty of Human Sciences, Waseda University, Saitama, Japan.
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Suzuki
authors.affiliation: Graduate School of Human Sciences, Waseda University, Saitama, Japan.
authors.forename: Toshimichi
authors.initials: T
authors.lastname: Ishijima
authors.affiliation: School of Human Movement Studies, University of Queensland, Brisbane, Australia.
authors.forename: Jonathan
authors.initials: J
authors.lastname: Peake
authors.affiliation: Faculty of Sport Sciences, Waseda University, Saitama, Japan.
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Higuchi
mesh_terms: D000328:Adult; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000097:blood / Q000378:metabolism / Q000494:pharmacology; D015444:Exercise / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology; D006727:Hormone Antagonists / Q000494:pharmacology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood* / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000097:blood / Q000378:metabolism; D008297:Male; D015735:Mifepristone / Q000494:pharmacology; D009000:Monocytes / Q000166:cytology / Q000378:metabolism*; D009638:Norepinephrine / Q000097:blood / Q000378:metabolism / Q000494:pharmacology; D011659:Pulmonary Gas Exchange; D054390:Receptors, CCR2 / Q000378:metabolism*; D013312:Stress, Physiological / Q000503:physiopathology; D013997:Time Factors
chemical_list: D006727:Hormone Antagonists; D018950:Lipopolysaccharide Receptors; D054390:Receptors, CCR2; D015735:Mifepristone; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine