The Effect of Restraint Stress on Glucocorticoid Receptors in Mouse Spleen Lymphocytes: Involvement of the Sympathetic Nervous System

Abstract

Objective: Reciprocal pathways of interaction between the nervous and immune systems during stress may be regulated by stress-induced circulating glucocorticoids that act via type II glucocorticoid receptors (GRs). The aim of the present study was to investigate the effect of restraint stress on GRs in lymphocytes and the role of the sympathetic system in this effect. Methods: We used male Balb/c mice which were adrenalectomized 3 days before exposure to restraint stress (4 h). Specific binding of ³H-dexamethasone (Dex) and the expression of GR protein were measured in the cytosol of spleen cells. Results: Restraint stress caused a significant increase in the maximal binding of ³H-Dex to GRs in the cytosol of spleen cells but not in the binding affinity. In correlation with this increase in binding, restraint stress caused an increase in the amount of GR protein. To establish the relation of the nervous system in this stress response, we blocked the autonomic innervations to the spleen with the ganglionic blocker chlorisondamine. This blocker abrogated the stress-induced increase in the binding of ³H-Dex to GRs and in the GR protein levels. Abrogation of the stress response was also achieved by blocking β-adrenergic receptors. Conclusion: These results suggest that stress-induced increase in the level of GRs is mediated by the sympathetic nervous system via β-adrenergic receptors. It is possible that stress modulation of lymphocyte GR levels may be implicated in the bidirectional communication between the nervous and the immune systems.

The protective effect of schisandra lignans on stress-evoked hepatic metastases of P815 tumor cells in restraint mice

“…Since CTL cells contributed to antitumor activity and the inhibition of cancer metastases , these results suggested that stress can facilitate cancer metastasis via a dysfunction of CTL cells. Numbers of studies reported that stress suppressed these immune functions (He et al, 2009b;Otten et al, 2010;Warner et al, 2010). Kurihara et al (2002) also reported that stress promoted tumorigenesis by reducing the number and impairing the lytic functions of NK cells.…”

Glucocorticoid Receptor Expression on Human B Cells in Response to Acute Heavy Resistance Exercise

“…The number of GCRs on mononuclear leukocytes correlates with hormone responsiveness [14] . Lymphocyte GCR levels are modulated by stress and communication between the nervous and immune systems [36] . More specifically, GCR expression is upregulated by catecholamines and corticosteroids [37,38] , hormones that increase during exercise.…”