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Title: Progenitor cells are mobilized by acute psychological stress but not beta-adrenergic receptor agonist infusion
Author(s): Natalie E. Riddell, Victoria E. Burns, Graham R. Wallace, Kate M. Edwards, Mark Drayson, Laura S. Redwine, Suzi Hong, Jack C. Bui, Johannes C. Fischer, Paul J. Mills and JOS A. BOSCH
Journal: Brain, Behavior, and Immunity
Year: 2015
State: accepted
DOI: 10.1016/j.bbi.2015.02.028
File URL: vuams-pubs/Riddell_2015.pdf
Keywords: Progenitor cells, Mobilization, Psychological stress, bAR-stimulation, Adrenergic
Abstract: Objectives: Stimuli that activate the sympathetic nervous system, such as acute psychological stress, rapidly invoke a robust mobilization of lymphocytes into the circulation. Experimental animal studies suggest that bone marrow-derived progenitor cells (PCs) also mobilize in response to sympathetic stimulation. Here we tested the effects of acute psychological stress and brief pharmacological b-adrenergic (bAR) stimulation on peripheral PC numbers in humans. Methods: In two studies, we investigated PC mobilization in response to an acute speech task (n = 26) and bAR-agonist (isoproterenol) infusion (n = 20). A subset of 8 participants also underwent the infusion protocol with concomitant administration of the bAR-antagonist propranolol. Flow cytometry was used to enumerate lymphocyte subsets, total progenitor cells, total haematopoietic stem cells (HSC), early HSC (multi-lineage potential), late HSC (lineage committed), and endothelial PCs (EPCs). Results: Both psychological stress and bAR-agonist infusion caused the expected mobilization of total monocytes and lymphocytes and CD8+ T lymphocytes. Psychological stress also induced a modest, but significant, increase in total PCs, HSCs, and EPC numbers in peripheral blood. However, infusion of a bAR-agonist did not result in a significant change in circulating PCs. Conclusion: PCs are rapidly mobilized by psychological stress via mechanisms independent of bARstimulation, although the findings do not exclude bAR-stimulation as a possible cofactor. Considering the clinical and physiological relevance, further research into the mechanisms involved in stress-induced PC mobilization seems warranted.

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