![]() Nurses experience a high incidence of workplace bullying and are at a higher risk of suicide than the general population. We conclude that workplace bullying promotes anxiety and threaten well-being through an ADRB2 associated mechanism. Genotyping with regard to the ADRB2 genotype rs1042714 CC vs CG/GG, on human saliva samples, showed that individuals with CC reported more anxiety following exposure to bullying behaviors as compared to the G carriers. Parallel cell culture work, which was performed to examine the direct effects of NE and DEX on ADRB2, demonstrated ADRB2 downregulation and MCP-1 upregulation in cultured EL-1 cells. The present study showed a clear association between reduced social interaction and increased level of circulating NE in rats previously exposed to repeated social defeat. Third, in a probability sample of 1052 Norwegian employees, the 9-item short version of the Negative Acts Questionnaire-Revised (S-NAQ) inventory, Hopkins Symptom Checklist and genotyping (SNP TaqMan assay) were used to examine the association between social stress in the form of workplace bullying and anxiety moderated by the ADRB2 genotype (rs1042714) in humans. Second, the direct effects of the stress-hormones NE and cortisol, i.e., synthetic dexamethasone (DEX), on the ADRB2 expression (qPCR) and monocyte chemoattractant protein-1 (MCP-1) release (immunoassay) was examined in cultured EL-1 cells. The analyses presented here focus on understanding the role of the β 2 -adrenergic receptors (ADRB2) on this association.įirst, a resident-intruder paradigm was used to investigate changes in circulating norepinephrine (NE) in rat serum induced by repeated social defeat and its relationship with subsequent social behavior. However, the understanding of the underlying biological mechanisms that may explain the relationship between exposure to bullying and such negative health outcomes is scarce. Several studies show that severe social stressors, e.g., in the form of exposure to workplace bullying in humans, is associated with negative mental health effects such as depression and anxiety among those targeted. We hope our shared datasets will facilitate further exploration of the motions tiggered by social stressors. Thus, our data show that the pituitary gene expression may be affected by social stress and that genetic variability in NRCAM intron 1 region influences stress-induced negative emotions. Also, genetic variability in this area was associated with altered stress response in male humans exposed to repeated social defeat in the form of abusive supervision. Among these, Neuronal cell adhesion molecule (Nrcam) showed reduced transcription and reduced DNA methylation in a region corresponding to intron 1 in human NRCAM. control rats, by RNA- and bisulfite DNA sequencing, we found regulation of genes involved in neuron morphogenesis and communication. Here, we examine the consequences of such stress (induced by resident-intruder paradigm) on the pituitary gland. Future research is needed to examine whether similar inflammatory changes also can explain the impact of social stress, such as bullying and harassment, among humans.Įnvironmental stressors such as repeated social defeat may initiate powerful activation of sub-conscious parts of the brain. Our results show that that the experience of social stress in the form of repeated social defeat in rats is a potent stressor that in myeloid cells in the spleen promotes persistent inflammatory changes. ![]() Subsequent analyses in the same cells showed that ARRB2 was negatively correlated with IL-6 following the stress exposure. In myeloid cells harvested from the spleen, we observed decreased expression of the β2-adrenergic receptor (ADRB2) and β-arrestin-2 (ARRB2), but increased expression of interleukin-6 (IL-6). An increased nuclear receptor subfamily group C number 1 (NR3C1) expression in the pituitary gland was also shown. The exposure to social stress induced decreased weight gain and increased locomotion. Gene expression in the pituitary gland, adrenal gland and myeloid cells isolated from the spleen was measured by qPCR. Variation in social interaction was observed manually, whereas locomotion was analyzed off-line by a purpose-made software. The day after the last stress exposure in the paradigm the data were analyzed. repeated social defeat, on behavior, hypothalamic-pituitary-adrenal (HPA)-axis and immune system.Ī resident-intruder paradigm, where an intruder rat was exposed to social stress by a dominant resident rat for 1 hour each day for 7 consecutive days was used. Here, we examine the effects of social stress in rats, i.e. Previous studies suggest that persistent exposure to social stress in mammals may be associated with multiple physiological effects.
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