Cortisol-induced CXCR4 augmentation mobilizes T lymphocytes after acute physical stress

Mitsuharu Okutsu, Kenji Ishii, Jun Niu Kai, Ryoichi Nagatomi

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

The aim of this study was to elucidate the mechanism responsible for lymphopenia after exercise. Seven young healthy men volunteered for this study. Peripheral blood mononuclear cells (PBMC) were cultured with cortisol and analyzed for C-X-C motif chemokine receptor 4 (CXCR4) expression by flow cytometry. To determine the effects of exercise, subjects performed exhaustive cycling exercise. PBMC were cultured with plasma obtained before and after the cycling exercise. Alternatively, PBMC obtained before and after exercise were cultured without plasma or glucocorticoid to examine whether PBMC were primed in vivo for CXCR4 expression. We analyzed cortisol- or plasma-treated PBMC to determine their ability to migrate through membrane filters in response to stromal cell-derived factor 1α/CXCL12. Cortisol dose-and time-dependently augmented CXCR4 expression on T lymphocytes, with <6 h of treatment sufficient to augment CXCR4 on T lymphocytes. Postexercise plasma also augmented CXCR4 expression. Cortisol or postexercise plasma treatment markedly enhanced migration of T lymphocytes toward CXCL12. Augmentation of CXCR4 on T lymphocytes by cortisol or plasma was effectively blocked by the glucocorticoid receptor antagonist RU-486. Thus exercise-elicited endogenous cortisol effectively augments CXCR4 expression on T lymphocytes, which may account for lymphopenia after exercise.

Original languageEnglish
Pages (from-to)R591-R599
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume288
Issue number3 57-3
DOIs
Publication statusPublished - 2005 Mar

Keywords

  • Chemokine receptor
  • Glucocorticoid
  • T cell distribution

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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