Effects of acute stress-induced immunomodulation on TH1/TH2 cytokine and catecholamine receptor expression in human...

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.

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.

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.

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.