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Acute stress increases monocyte levels and modulates receptor expression in healthy females
- Publication Year :
- 2021
- Publisher :
- Elsevier, 2021.
-
Abstract
- 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.
- Subjects :
- 0301 basic medicine
Receptor expression
Immunology
Gene Expression
Activation
Monocytes
Cortisol
Flow cytometry
Colony stimulating factor 1 receptor
Mice
03 medical and health sciences
Behavioral Neuroscience
0302 clinical medicine
Immune system
medicine
Animals
Responses
Receptor
Glucocorticoids
Inflammation
Innate immune system
medicine.diagnostic_test
Endocrine and Autonomic Systems
business.industry
Depression
Monocyte
Immune cells
Cold pressor test
Brain
030104 developmental biology
medicine.anatomical_structure
Psychological stress
Female
Recruitment
business
030217 neurology & neurosurgery
Subjects
Details
- Language :
- English
- Database :
- OpenAIRE
- Accession number :
- edsair.doi.dedup.....4ebdd1508787215d2bc4186bd2eb1ce2