Beta-adrenergic blockade blunts inflammatory and antiviral/antibody gene expression responses to acute psychosocial stress

Abstract Objective: The impact of psychosocial stress on a variety of negative health outcomes is well documented, with current research efforts directed at possible mechanisms. Here, we focused on a potential mechanism involving differential expression of mRNA and microRNA in response to acute psychosocial stress. We utilized a validated behavioral paradigm, the Trier Social Stress Test (TSST), to induce acute psychosocial stress in a cohort of volunteers. Stress reactivity was assessed repeatedly during the TSST using saliva samples that were analyzed for levels of cortisol. Peripheral blood mononuclear cells were extracted from blood drawn at baseline and at two time points following the stress paradigm. Total RNA was extracted, and mRNA and microRNA microarrays were utilized to assess within-subject changes in gene expression between baseline and the two post-stressor time points. Results: For microarray gene expression analysis, we focused on 12 participants who showed a robust cortisol response to the task, as an indicator of robust HPA-axis activation. We discovered a set of mRNAs and miRNAs that exhibited dynamic expression change in response to the TSST in peripheral blood mononuclear cells, further characterizing the link between psychosocial stress and cellular response mechanisms.

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Early-life adversity is associated with differential gene expression in response to acute psychological stress: preliminary findings

10.1101/727180 ◽

2019 ◽

Author(s):

Idan Shalev ◽

Waylon J. Hastings ◽

Laura Etzel ◽

Salomon Israel ◽

Michael A. Russell ◽

...

Keyword(s):

Gene Expression ◽

Experimental Design ◽

Inflammatory Cytokines ◽

Early Life ◽

Psychosocial Stress ◽

Group Status ◽

Early Life Adversity ◽

Acute Psychosocial Stress ◽

Physiological Systems ◽

Pro Inflammatory Cytokines

AbstractObjectiveExposure to early-life adversity (ELA) can result in long-term changes to physiological systems, which predispose individuals to negative health outcomes. This biological embedding of stress-responsive systems may operate via dysregulation of physiological resources in response to common stressors. The present study used a novel experimental design to test how young adults’ exposure to ELA influence neuroendocrine and inflammatory responses to acute stress.Materials and methodsParticipants were 12 males (mean age= 21.25), half of whom endorsed at least three significant adverse events up to age 18 years (‘ELA group’), and half who confirmed zero (‘controls’). Using a randomized within-subjects, between-groups experimental design, we induced acute psychosocial stress (Trier Social Stress Test, TSST), and included a no-stress control condition one week apart. During these sessions, we obtained repeated measurements of physiological reactivity, gene expression of NR3C1, FKBP5 and NFKB1, and plasma levels of pro-inflammatory cytokines (IL-1β, IL-6, IL-8 and TNFα) over a 4-hour window post-test.ResultsThe ELA group evinced significantly higher cortisol response and lower NR3C1 gene expression in response to the TSST compared with controls, while no differences were observed in the no-stress condition. Cortisol and group status interacted such that increase in cortisol predicted increase in both NR3C1 and NFKB1 expression among controls, but decrease in the ELA group. For pro-inflammatory cytokines, only IL-6 increased significantly in response to the TSST, with no differences between the two groups.ConclusionOverall, we provide preliminary findings for the biological embedding of stress via a dynamic and dysregulated pattern evidenced in response to acute psychosocial stress. ELA may program physiological systems in a maladaptive manner more likely to manifest during times of duress, predisposing individuals to the negative health consequences of everyday stressors. Future studies with larger sample size including both males and females are needed to replicate these findings.

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Retrieval-induced forgetting under psychosocial stress: No reduction by delayed stress and beta-adrenergic blockade

Neurobiology of Learning and Memory ◽

10.1016/j.nlm.2014.01.010 ◽

2014 ◽

Vol 110 ◽

pp. 35-46 ◽

Cited By ~ 3

Author(s):

Laura Dreifus ◽

Harald Engler ◽

Johanna Kissler

Keyword(s):

Psychosocial Stress ◽

No Reduction ◽

Adrenergic Blockade ◽

Beta Adrenergic ◽

Induced Forgetting

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Integrated microRNA and mRNA gene expression in peripheral blood mononuclear cells in response to acute psychosocial stress: a repeated-measures within-subject pilot study

BMC Research Notes ◽

10.1186/s13104-021-05635-3 ◽

2021 ◽

Vol 14 (1) ◽

Author(s):

Magdalena Maria Jurkiewicz ◽

Anett Mueller-Alcazar ◽

Dirk Alexander Moser ◽

Indralatha Jayatilaka ◽

Anatoly Mikhailik ◽

...

Keyword(s):

Gene Expression ◽

Peripheral Blood Mononuclear Cells ◽

Peripheral Blood ◽

Psychosocial Stress ◽

Mononuclear Cells ◽

Peripheral Blood Mononuclear ◽

Time Points ◽

Blood Mononuclear Cells ◽

The Impact ◽

Acute Psychosocial Stress

Abstract Objective The impact of psychosocial stress on a variety of negative health outcomes is well documented, with current research efforts directed at possible mechanisms. Here, we focused on a potential mechanism involving differential expression of mRNA and microRNA in response to acute psychosocial stress. We utilized a validated behavioral paradigm, the Trier Social Stress Test (TSST), to induce acute psychosocial stress in a cohort of volunteers. Stress reactivity was assessed repeatedly during the TSST using saliva samples that were analyzed for levels of cortisol. Peripheral blood mononuclear cells were extracted from blood drawn at baseline and at two time points following the stress paradigm. Total RNA was extracted, and mRNA and microRNA microarrays were utilized to assess within-subject changes in gene expression between baseline and the two post-stressor time points. Results For microarray gene expression analysis, we focused on 12 participants who showed a robust cortisol response to the task, as an indicator of robust HPA-axis activation. We discovered a set of mRNAs and miRNAs that exhibited dynamic expression change in response to the TSST in peripheral blood mononuclear cells, further characterizing the link between psychosocial stress and cellular response mechanisms.

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