Effects of Acute Stress-Induced Immunomodulation on Th1/Th2 Cytokine and Catecholamine Receptor Expression in Human Peripheral Blood Cells

Abstract

Aims: There is evidence that psychological stress can modulate immune functions. It has been hypothesized that acute stressors can affect both immune balance (including Th1 and Th2 cytokines) and expression of stress hormone receptors. This study investigated the impact of an acute stressor on gene expressions of glucocorticoid receptor (GR), and β₂-adrenergic receptor (β2AR) in leukocytes. The effect on T regulatory cells (Treg), regulatory cytokines IL-10 and TGF-β, Th1 and Th2 cytokines and their receptors IFN-γR and IL-4R was also studied. Method: Fourteen normal volunteers completed an acute laboratory stressor, and blood samples were collected before, immediately after, and 1, 2, 6 and 24 h after completion of the tasks. Cytokine production and Treg were determined by flow cytometry. Gene expressions of receptors were analyzed by real-time PCR. Results: IFN-γ was increased immediately and 1 h after stressor (p < 0.05, respectively) and upregulation of IFN-γR mRNA was noted at 2, 6 and 24 h (p < 0.01, respectively). IL-10 was decreased at 2 h (p < 0.01). There were no significant changes in post-task IL-4R, Treg, or TGF-β. β2AR mRNA was increased at 2, 6 and 24 h (p < 0.01, respectively). On the other hand, no significant alterations were observed in GR expression. Conclusion: An acute stressor increased Th1 cytokine production and its receptor expression. β2AR but not GR was significantly increased after an acute stressor, which supports the hypothesis that catecholamine-mediated signal pathways in communication with the central nervous and immune systems play a fundamental role in acute stress-mediated immune alterations.

Regulation of Differentiation and Function of Helper T Cells by Lymphocyte-Derived Catecholamines via α₁- and β₂-Adrenoceptors

“…These facts support that in mediating the CA immunomodulation, α 1 -ARs and β 2 -ARs play a dominant role. Several studies, including that from our laboratory, have demonstrated the presence of AR subtypes on immunocytes and their various functions in mediating immunomodulation of CAs [23,24,25,29,30,31,44]. Thus, a possible mechanism underlying the modulation of lymphocyte differentiation and function by the lymphocyte-derived CAs is established.…”

Th1/Th2/Th17 cells imbalance in patients with asthma with and without psychological symptoms

“…As Xiang reported, acute stressor augmented the production of Th1 cytokine in normal volunteers through the protective immune response. 25 Stress and anxiety enhanced late-phase responses and promoted hyperresponsiveness in patients with allergic rhinitis. 43 Cohen et al 44 found that chronic psychological stress dysregulated the inflammatory response.…”

“…22 Neuroimmunology of psychological symptoms is dominated by "immune activation" hypothesis and "immune suppression" hypothesis. 23 The balance of Th cells is shifted toward Th1 cells 24,25 and Th17 cells 26,27 in depression or anxiety.…”

The Impact of Self-Reported Psychological Stress Levels on Changes to Peripheral Blood Immune Biomarkers in Recreational Marathon Runners during Training and Recovery

“…Data on the effects of different types of stress on Tr1 cells are also limited. We recently reported that the percentage of Tr1 cells is lower 2 h after administration of an acute psychological stressor in a human stress model [43]. Th3 cells produce TGFβ, which is an important factor in the differentiation of regulatory cell phenotypes, including classic FoxP3 + regulatory T cells (Treg) and Th17 cells [44].…”