Acute stress increases monocyte levels and modulates receptor expression in healthy females

• Published in: Brain, behavior, and immunity Vol. 94; pp. 463 - 468
• Main Authors: van de Wouw, Marcel, Sichetti, Marzia, Long-Smith, Caitriona M., Ritz, Nathaniel L., Moloney, Gerard M., Cusack, Anne-Marie, Berding, Kirsten, Dinan, Timothy G., Cryan, John F.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01-05-2021
• Subjects: Acute stress; Human; Immune system; Monocytes; Human; Monocytes; Acute stress; Immune system
• ISSN: 0889-1591; 1090-2139
• DOI: 10.1016/j.bbi.2021.03.005

•It has been shown that acute stress alters immune cell levels (i.e., monocytes) in rodents.•Here it is shown that acute stress increases monocyte levels in healthy females.•This is paired with alterations in the expression of specific receptors on monocytes.
There has been a growing recognition of the involvement of the immune system in stress-related disorders. Acute stress leads to the activation of neuroendocrine systems, which in turn orchestrate a large-scale redistribution of innate immune cells, such as monocytes. Even though acute stress/monocyte interactions have been well-characterized in mice, this is not the case for humans. As such, this study aimed to investigate whether acute stress modulates blood monocyte levels in a subtype-dependent manner and whether the receptor expression of stress-related receptors is affected in humans. Blood was collected from healthy female volunteers at baseline and 1 h after the socially evaluated cold pressor test, after which blood monocyte levels and receptor expression were assessed by flow cytometry. Our results reveal a stress-induced increase in blood monocyte levels, which was independent of monocyte subtypes. Furthermore, colony stimulating factor 1 receptor (CSF-1R) and CD29 receptor expression was increased, while CD62L showed a trend towards increased expression. These results provide novel insights into how acute stress affects the innate immune system.