Glucocorticoids enhance the in vivo migratory response of human monocytes

Highlights • We transiently exposed humans to stress concentrations of cortisol. • Cortisol exposure increased mRNA for adhesion and chemotaxis molecules in monocytes. • Cortisol exposure increased expression of CCR2 on monocytes. • Cortisol exposure increased macrophages and neutrophils in inflamma...

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Veröffentlicht in:	Brain, behavior, and immunity behavior, and immunity, 2016-05, Vol.54, p.86-94
Hauptverfasser:	Yeager, Mark P, Pioli, Patricia A, Collins, Jane, Barr, Fiona, Metzler, Sara, Sites, Brian D, Guyre, Paul M
Format:	Artikel
Sprache:	eng
Schlagworte:	Allergy and Immunology CCR2 Cell Movement - drug effects Cell Movement - immunology Chemokine CCL2 - pharmacology Chemotaxis, Leukocyte - drug effects Cortisol CX3CR1 Female Humans Hydrocortisone - blood Hydrocortisone - pharmacology Inflammation - metabolism IκBα Macrophage Macrophages - metabolism Macrophages - physiology Male Monocyte Monocytes - cytology Monocytes - drug effects Monocytes - metabolism Neutrophils - metabolism Neutrophils - physiology Psychiatry Receptors, CCR2 - biosynthesis Receptors, CCR2 - immunology RNA, Messenger - metabolism Stress Stress, Physiological Up-Regulation - drug effects
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Zusammenfassung:	Highlights • We transiently exposed humans to stress concentrations of cortisol. • Cortisol exposure increased mRNA for adhesion and chemotaxis molecules in monocytes. • Cortisol exposure increased expression of CCR2 on monocytes. • Cortisol exposure increased macrophages and neutrophils in inflammatory exudate. • A model of delayed cortisol augmentation of inflammation is presented.
ISSN:	0889-1591 1090-2139
DOI:	10.1016/j.bbi.2016.01.004